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ID	THPP_ID	Therapeutic Name	Sequence	Molecular Weight	Chemical Formula	Isoelectric Point	Hydrophobicity	Melting Point	Half Life	Description	Disease/Indication	Pharmacodynamics	Mechanism of Action	Toxicity	Metabolism	Absorption	Volume of Distribution	Clearance	Categories	Patent Number	Date of Issue	Date of Expiry	Drug Interaction	Target	Brand Name	Company	Brand Description	Prescribed for	Chemical Name	Formulation	Physical Appearance	Route of Administation	Recommended Dosage	Contraindication	Side Effects	Useful Links 1	Useful Links 2	Remarks
10409	Th1067	Daptomycin	NA	1620.693	C72H101N17O26	NA	NA	NA	Normal range: 7.5-9 hours 27.83 ± 14.85 hours in patients with creatinine clearance <30 mL/min	Daptomycin is a lipopeptide antibiotic that kills susceptible gram positive bacteria by disrupting their membrane potential. It is a naturally-occurring compound found in the soil bacterium <i>Streptomyces roseosporus</i>. Antibiotics are used in the treatment of infections caused by bacteria. They work by killing bacteria or preventing their growth. Daptomycin will not work for colds, flu, or other virus infections. It was approved in September 2003 for the treatment of complicated skin and soft tissue infections. It has a safety profile similar to other agents commonly administered to treat gram-positive infections.	For the treatment of complicated skin and skin structure infections caused by susceptible strains of Gram-positive microorganisms.	Daptomycin is a 13 member amino acid cyclic lipopeptide antibiotic active against Gram-positive bacteria only. It has proven in vitro activity against enterococci (including glycopeptide-resistant Enterococci (GRE)), staphylococci (including methicillin-resistant <i>Staphylococcus aureus</i>), streptococci and corynebacteria. Daptomycin is derived from the fermentation product of Streptomyces roseosporus.	Daptomycin appears to bind or insert into the outer membrane of gram positive bacteria. The binding and integration of daptomycin into the cell membrane is calcium dependent. Calcium ions cause a conformational change in daptomycin, augmenting its amphipathicity (hydrophilic head group and hydrophobic tail group), leading to incorporation into the cell membrane. This binding causes rapid depolarisation, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death. The bactericidal activity of daptomycin is concentration-dependent. There is in vitro evidence of synergy with ÃŽÂ²-lactam antibiotics.	NA	Minor amounts of three oxidative metabolites and one unidentified compound have been detected in urine. The site of metabolism has not been identified.	NA	0.1 L/Kg [healthy adult subjects]	As daptomycin is primarily renally excreted, patients with mild, moderate, and severe renal impairment had reduced total plasma clearance 9, 22, and 46 percent lower than healthy controls, respectively. Daptomycin clearance was also lower in obese (15-23%) and geriatric (aged 75 and older, by 35%) patients, whereas it tended to be higher in pediatric patients, even when normalized for body weight	Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Antibacterials for Systemic Use, Antiinfectives for Systemic Use, Cyclic Lipopeptides, Drugs that are Mainly Renally Excreted, Lipids, Lipopeptide Antibacterial, Lipopeptides, P-glycoprotein substrates, Peptides, Peptides, Cyclic	US6468967	22-Oct-2002	24-Sep-2019	NA	Cytoplasmic membrane	CUBICIN	Cubist Pharmaceuticals, Inc	Cubist Pharmaceuticals, Inc	Complicated skin and skin structure infections (cSSSI), Staphylococcus aureus bloodstream infections (bacteremia), including those with right-sided infective endocarditis, caused by methicillin-susceptible and methicillin-resistant isolates	N-decanoyl-L-tryptophyl-Dasparaginyl-L-aspartyl-L-threonylglycyl-L-ornithyl-L-aspartyl-D-alanyl-L-aspartylglycyl-Dseryl-threo-3-methyl-L-glutamyl-3-anthraniloyl-L-alanineÃ‚Â ÃŽÂµ1-lactone	CUBICIN contains 500 mg of daptomycin and reconstituted with 0.9% sodium chloride injection. The only inactive ingredient is sodium hydroxide, which is used in minimal quantities for pH adjustment.	CUBICIN is a Sterile, preservative-free, pale yellow to light brown, lyophilized cake containing approx 500 mg of daptomycin	Intravenous (Intravenous) Injection	CUBICIN 4 mg/kg should be administered intravenously in 0.9% sodium chloride injection once every 24 hours for 7 to 14 days. Staphylococcus aureus Bloodstream Infections (Bacteremia) - CUBICIN 6 mg/kg should be administered intravenously in 0.9% sodium chloride injection once every 24 hours for 2 to 6 weeks.	CUBICIN is contraindicated in patients with known hypersensitivity to daptomycin	fatigue, weakness, rigors, flushing, hypersensitivity, leukocytosis, thrombocytopenia, thrombocytosis, eosinophilia, increased International Normalized Ratio (INR), supraventricular arrhythmia, eczema, abdominal distension, stomatitis, jaundice, increased serum lactate dehydrogenase, hypomagnesemia, increased serum bicarbonate, electrolyte disturbance, myalgia, muscle cramps, muscle weakness, arthralgia, vertigo, mental status change, paresthesia, taste disturbance, eye irritation	Link	NA	NA
10410	Th1067	Daptomycin	NA	1620.693	C72H101N17O26	NA	NA	NA	0.51 ± 6.51 hours in hemodialysis patients	Daptomycin is a lipopeptide antibiotic that kills susceptible gram positive bacteria by disrupting their membrane potential. It is a naturally-occurring compound found in the soil bacterium <i>Streptomyces roseosporus</i>. Antibiotics are used in the treatment of infections caused by bacteria. They work by killing bacteria or preventing their growth. Daptomycin will not work for colds, flu, or other virus infections. It was approved in September 2003 for the treatment of complicated skin and soft tissue infections. It has a safety profile similar to other agents commonly administered to treat gram-positive infections.	For the treatment of complicated skin and skin structure infections caused by susceptible strains of Gram-positive microorganisms.	Daptomycin is a 13 member amino acid cyclic lipopeptide antibiotic active against Gram-positive bacteria only. It has proven in vitro activity against enterococci (including glycopeptide-resistant Enterococci (GRE)), staphylococci (including methicillin-resistant <i>Staphylococcus aureus</i>), streptococci and corynebacteria. Daptomycin is derived from the fermentation product of Streptomyces roseosporus.	Daptomycin appears to bind or insert into the outer membrane of gram positive bacteria. The binding and integration of daptomycin into the cell membrane is calcium dependent. Calcium ions cause a conformational change in daptomycin, augmenting its amphipathicity (hydrophilic head group and hydrophobic tail group), leading to incorporation into the cell membrane. This binding causes rapid depolarisation, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death. The bactericidal activity of daptomycin is concentration-dependent. There is in vitro evidence of synergy with ÃŽÂ²-lactam antibiotics.	NA	Minor amounts of three oxidative metabolites and one unidentified compound have been detected in urine. The site of metabolism has not been identified.	NA	0.1 L/Kg [healthy adult subjects]	As daptomycin is primarily renally excreted, patients with mild, moderate, and severe renal impairment had reduced total plasma clearance 9, 22, and 46 percent lower than healthy controls, respectively. Daptomycin clearance was also lower in obese (15-23%) and geriatric (aged 75 and older, by 35%) patients, whereas it tended to be higher in pediatric patients, even when normalized for body weight	Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Antibacterials for Systemic Use, Antiinfectives for Systemic Use, Cyclic Lipopeptides, Drugs that are Mainly Renally Excreted, Lipids, Lipopeptide Antibacterial, Lipopeptides, P-glycoprotein substrates, Peptides, Peptides, Cyclic	USRE39071	18-Apr-2006	15-Jun-2016	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA
10411	Th1067	Daptomycin	NA	1620.693	C72H101N17O26	NA	NA	NA	27.56 ± 4.53 hours in continuous ambulatory peritoneal dialysis (CAPD) patients	Daptomycin is a lipopeptide antibiotic that kills susceptible gram positive bacteria by disrupting their membrane potential. It is a naturally-occurring compound found in the soil bacterium <i>Streptomyces roseosporus</i>. Antibiotics are used in the treatment of infections caused by bacteria. They work by killing bacteria or preventing their growth. Daptomycin will not work for colds, flu, or other virus infections. It was approved in September 2003 for the treatment of complicated skin and soft tissue infections. It has a safety profile similar to other agents commonly administered to treat gram-positive infections.	For the treatment of complicated skin and skin structure infections caused by susceptible strains of Gram-positive microorganisms.	Daptomycin is a 13 member amino acid cyclic lipopeptide antibiotic active against Gram-positive bacteria only. It has proven in vitro activity against enterococci (including glycopeptide-resistant Enterococci (GRE)), staphylococci (including methicillin-resistant <i>Staphylococcus aureus</i>), streptococci and corynebacteria. Daptomycin is derived from the fermentation product of Streptomyces roseosporus.	Daptomycin appears to bind or insert into the outer membrane of gram positive bacteria. The binding and integration of daptomycin into the cell membrane is calcium dependent. Calcium ions cause a conformational change in daptomycin, augmenting its amphipathicity (hydrophilic head group and hydrophobic tail group), leading to incorporation into the cell membrane. This binding causes rapid depolarisation, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death. The bactericidal activity of daptomycin is concentration-dependent. There is in vitro evidence of synergy with ÃŽÂ²-lactam antibiotics.	NA	Minor amounts of three oxidative metabolites and one unidentified compound have been detected in urine. The site of metabolism has not been identified.	NA	0.1 L/Kg [healthy adult subjects]	As daptomycin is primarily renally excreted, patients with mild, moderate, and severe renal impairment had reduced total plasma clearance 9, 22, and 46 percent lower than healthy controls, respectively. Daptomycin clearance was also lower in obese (15-23%) and geriatric (aged 75 and older, by 35%) patients, whereas it tended to be higher in pediatric patients, even when normalized for body weight	Agents Causing Muscle Toxicity, Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Antibacterials for Systemic Use, Antiinfectives for Systemic Use, Cyclic Lipopeptides, Drugs that are Mainly Renally Excreted, Lipids, Lipopeptide Antibacterial, Lipopeptides, P-glycoprotein substrates, Peptides, Peptides, Cyclic	CA2344318	4-Jul-2006	24-Sep-2019	NA	B-lymphocyte antigen CD20,Low affinity immunoglobulin gamma Fc region receptor III-B,Complement C1r subcomponent,Complement C1q subcomponent subunit A,Complement C1q subcomponent subunit B,Complement C1q subcomponent subunit C,Low affinity immunoglobulin gamma Fc region receptor III-A,Complement C1s subcomponent,High affinity immunoglobulin gamma Fc receptor I,Low affinity immunoglobulin gamma Fc region receptor II-a,Low affinity immunoglobulin gamma Fc region receptor II-b,Low affinity immunoglobulin gamma Fc region receptor II-c	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA
10453	Th1081	Antithymocyte globulin	NA	NA	NA	NA	NA	61 (FAB fr	2-3 days	Polyclonal rabbit anti-thymocyte globulin. Used to suppresses certain types of immune cells ascribed to acute organ rejection in transplant patients by selective depletion of T-cells.	For prevention of renal transplant rejection	Antithymocyte Globulin (ATG)is a concentrated anti-human T-lymphocyte immunoglobulin preparation derived from rabbits after immunization with a T-lympoblast cell line. ATG is an immunosuppressive product for the prevention and treatment of acute rejection following organ transplantation. ATG reduces the host immune response against tissue transplants or organ allografts.	Binds to multiple, T-cell specific antigens leading to T-lymphocyte cell death via complement mediated cytotoxicity or apoptosis.	Not known whether ATG (rabbit) distributes into human milk; however, other immunoglobulins are distributed into human milk.	Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production.	T-cell depletion usually observed within 1 day after initiating therapy. Average 21.5 and 87 mcg/mL 4–8 hours post-infusion after first and last IV doses, respectively, when given for 7–11 days.	NA	NA	Immunologic Factors and Immunosuppressive Agents	NA	NA	NA	Canakinumab results in increased immunosuppressive effects; increases the risk of infection	NA	Antithymocyte globulin	Pfizer	Pfizer	NA	NA	Powder for injection 25 mg vials	NA	Intravenous infusion	Usual Adult Dose for Renal Transplant: 1.5 mg/kg/day by IV infusion for 7 to 14 days. Anti-thymocyte globulin (rabbit) should be infused over a minimum of 6 hours for the first infusion and over at least 4 hours on subsequent days of therapy. Premedication with corticosteroids, acetaminophen, and/or an antihistamine 1 hour prior to the infusion is recommended and may reduce the incidence and intensity of side effects during the infusion.	Acute viral illness; hypersensitivity to leporine proteins; previous hypersensitivity to anti-thymocyte globulin.	NA	NA	NA	NA
10454	Th1081	Antithymocyte globulin	NA	NA	NA	NA	NA	62 (FAB fr	2-3 days	Polyclonal rabbit anti-thymocyte globulin. Used to suppresses certain types of immune cells ascribed to acute organ rejection in transplant patients by selective depletion of T-cells.	For prevention of renal transplant rejection	Antithymocyte Globulin (ATG)is a concentrated anti-human T-lymphocyte immunoglobulin preparation derived from rabbits after immunization with a T-lympoblast cell line. ATG is an immunosuppressive product for the prevention and treatment of acute rejection following organ transplantation. ATG reduces the host immune response against tissue transplants or organ allografts.	Binds to multiple, T-cell specific antigens leading to T-lymphocyte cell death via complement mediated cytotoxicity or apoptosis.	Not known whether ATG (rabbit) distributes into human milk; however, other immunoglobulins are distributed into human milk.	Most likely removed by opsonization via the reticuloendothelial system when bound to T lymphocytes, or by human antimurine antibody production.	T-cell depletion usually observed within 1 day after initiating therapy. Average 21.5 and 87 mcg/mL 4–8 hours post-infusion after first and last IV doses, respectively, when given for 7–11 days.	NA	NA	Immunologic Factors and Immunosuppressive Agents	NA	NA	NA	Rilonacept results in increased immunosuppressive effects; increases the risk of infection	NA	Thymoglobulin	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA
10556	Th1108	Pegaptanib	NA	541.6	C22H44N3O10P	NA	NA	NA	10 Ã‚Â± 4 days	It is a polynucleotide aptamer, which specifically binds to VEGF 165, a protein that plays a critical role in angiogenesis and increased permeability of blood vessels; two of the primary pathological processes responsible for vision loss associated with neovascular AMD. [Wikipedia]	For the treatment of neovascular (wet) age-related macular degeneration.	Pegaptanib is a selective vascular endothelial growth factor (VEGF) antagonist. VEGF is a secreted protein that selectively binds and activates its receptors located primarily on the surface of vascular endothelial cells. VEGF induces angiogenesis, and increases vascular permeability and inflammation, all of which are thought to contribute to the progression of the neovascular (wet) form of age-related macular degeneration (AMD), a leading cause of blindness. VEGF has been implicated in blood retinal barrier breakdown and pathological ocular neovascularization.	Pegaptanib binds to the major pathological VEGF isoform, extracellular VEGF165, thereby inhibiting VEGF165 binding to its VEGF receptors. The inhibition of VEGF164, the rodent counterpart of human VEGF165, was effective at suppressing pathological neovascularization.	It is not known if pegaptanib is safe in pregnant women or if it is excreted in breast milk. Likewise, no studies have been done in the pediatric population. Most adverse events elated to the drug are ocular however non-ocular adverse events related to the drug or the injection procedure also occurred, among which headaches and rhinorrhoea appeared in more than 1% of patients. Pegaptanib is contraindicated when the patient has an ocular or periocular infection.	Based on preclinical data, pegaptanib is metabolized by endo- and exonucleases.	In animals, pegaptanib is slowly absorbed into the systemic circulation from the eye after intravitreous administration.	It is distributed into vitreous fluid, retina, aqueous fluid, and kidneys. As well, it has been shown to cross the placenta in mice but whether or not it crosses the placenta in humans is unknown.	NA	Intended for the prevention of respiratory distress syndrome (RDS) in premature infants at high risk for RDS.	NA	NA	NA	NA	Vascular endothelial growth factor A	Macugen	Gilead Sciences	Gilead Sciences	Macugen is indicated for the treatment of neovascular (wet) age-related macular degeneration.	NA	Macugen is supplied in a single-dose, pre-filled syringe and is formulated as a 3.47 mg/mL solution, measured as the free acid form of the oligonucleotide. The active ingredient is 0.3 mg of the free acid form of the oligonucleotide without polyethylene glycol, in a nominal volume of 90 ÃŽÂ¼L. This dose is equivalent to 1.6 mg of pegaptanib sodium (pegylated oligonucleotide) or 0.32 mg when expressed as the sodium salt form of the oligonucleotide moiety. The product is a sterile, clear, preservative-free solution containing sodium chloride, monobasic sodium phosphate monohydrate, dibasic sodium phosphate heptahydrate, hydrochloric acid, and/or sodium hydroxide to adjust the pH and water for injection.	Sterile, aqueous solution containing pegaptanib sodium for intravitreous injection	Intravitreal Injection ONLY	Macugen 0.3 mg should be administered once every six weeks into the eye to be treated.	Ocular or Periocular Infections: Macugen is contraindicated in patients with ocular or periocular infections.Hypersensitivity to pegaptanib sodium or any other excipient in this product.	The most frequently reported adverse events in patients treated with Macugen 0.3 mg for up to two years were anterior chamber inflammation, blurred vision, cataract, conjunctival hemorrhage, corneal edema, eye discharge, eye irritation, eye pain, hypertension, increased intraocular pressure (IOP), ocular discomfort, punctate keratitis, reduced visual acuity, visual disturbance, vitreous floaters, and vitreous opacities; Ocular: blepharitis, conjunctivitis, photopsia, vitreous disorder.; Non-Ocular: bronchitis, diarrhea, dizziness, headache, nausea, urinary tract infection.	Link	NA	NA
10564	Th1115	Teicoplanin	NA	1879.658	C88H97Cl2N9O33	NA	NA	NA	70-100 hrs	Glycopeptide antibiotic. It is a mixture of several compounds majorly teicoplanin A2-1 through A2-5, along with four minor ones, teicoplanin RS-1 through RS-4. They all share a same glycopeptide core, referred to as teicoplanin A3-1, which is a fused ring structure bound by two carbohydrates (mannose and N-acetylglucosamine). The components also contain a third carbohydrate moiety, ÃŽÂ²-D-glucosamine, and differ only by the length and conformation of a side chain attached to it.	For the treatment of bacterial infections caused by susceptible microorganisms.	Teicoplanin is an antibiotic used in the prophylaxis and treatment of serious infections caused by Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus and Enterococcus faecalis. It is a glycopeptide antiobiotic extracted from Actinoplanes teichomyceticus, with a similar spectrum of activity to vancomycin. Its mechanism of action is to inhibit bacterial cell wall synthesis. Oral teicoplanin has been demonstrated to be effective in the treatment of pseudomembranous colitis and Clostridium difficile-associated diarrhoea, with comparable efficacy to vancomycin.	Teicoplanin inhibits peptidoglycan polymerization, resulting in inhibition of bacterial cell wall synthesis and cell death.	NA	NA	NA	NA	NA	Anti-Bacterial Agents	NA	NA	NA	NA	D-Ala-D-Ala moiety of NAM/NAG peptide subunits of peptidoglycan	Targocid	NPS Pharmaceuticals	NPS Pharmaceuticals	Acts against Gram-postive bacteria including methicillin-resistant Staphylococcus aureus and Enterococcus fecalis. Targocid is indicated in adults and in children from birth for the parenteral treatment of the following infections skin and soft tissue infections, bone and joint infections, hospital acquired pneumonia, community acquired pneumonia, complicated urinary tract infections, infective endocarditis, continuous ambulatory peritoneal dialysis (CAPD), bacteraemia that occurs in association with any of the indications listed above. Targocid is also indicated as an alternative oral treatment for Clostridium difficile infection-associated diarrhoea and colitis.	NA	Each vial of Targocid injection contains 400 mg teicoplanin. The glass vial also contains an inactive ingredient, sodium chloride which is included to minimise stinging and pain when the injection is administered. There are no dyes, gluten or preservatives in Targocid injection.	Light yellow solid	Intramuscular, Intravenous	NA	Serious, life-threatening hypersensitivity reactions, sometimes fatal, have been reported with teicoplanin (e.g. anaphylactic shock). If an allergic reaction to teicoplanin occurs, treatment should be discontinued immediately and appropriate emergency measures should be initiated. Teicoplanin must be administered with caution in patients with known hypersensitivity to vancomycin, as crossed hypersensitivity reactions, including fatal anaphylactic shock, may occur. However, a prior history of red man syndrome with vancomycin is not a contraindication to the use of teicoplanin.	Infusion related reactions, Severe bullous reactions, Nephrotoxicity, Ototoxicity, Superinfection	Link	NA	NA
10577	Th1118	Sulodexide	NA	5000-8000	NA	NA	NA	NA	elimination half-life was 11.7 Ã‚Â± 2.0 h by IV route	A mixture of glycosaminoglycans (GAGs), composed of dermatan sulfate (DS) and fast moving heparin (FMH).	For the treatment of thrombosis. Also investigated for use/treatment in diabetic kidney disease, and neuropathy (diabetic).	The low molecular weight of both sulodexide fractions allows for extensive oral absorption compared to unfractionated heparin. The pharmacological effects of sulodexide differ substantially from other glycosaminoglycans and are mainly characterized by a prolonged half-life and reduced effect on global coagulation and bleeding parameters. Due to the presence of both glycosaminoglycan fractions, sulodexide potentiates the antiprotease activities of both antithrombin III and heparin cofactor II simultaneously.	Thrombin inhibition produced by sulodexide is due to the additive effect of its components, namely, heparin cofactor II (HCII) catalysis by dermatan sulfate and antithrombin-III catalysis by fast moving heparin (FMH).	Sulodexide seems to be well tolerated. Most adverse effects reported are related to the GI system and seem to be transient in nature. Among others adverse reactions are diarrhea, epigastralgia, dyspepsia, heartburn and dizziness. Allergic reactions, such as skin rash, have also been reported but are very rare.	It is mainly metabolized in the liver.	Sulodexide can be administered via the oral route, IV and IM routes. After oral dosing, the absorption rate being equivalent, the bioavailability is 40-60%. either calculated from the fast-moving heparin fraction or from the dermatan fraction. Bioavailability following IM administration is approximately 90%. After a rapid absorption in the intestine, the dermatan and heparin components start to appear in the plasma. Sulodexide is degraded after ingestion and loses its sulfate groups and both sulfated and unsulfated groups circulate in the blood for up to 24hours. AUC=22.83+/-4.44mg.h/L.	Cmax=516+/-77.54ng/mL, Tmax=1.33+/-0.58h, Vd=71.24+/-14.06L (b phase). Sulodexide reaches high concentrations in the plasma and is widely distributed in the endothelial layer. Binding to endothelial cell receptors in arteries and veins contributes to its rapid distribution profile.	2.70+/-0.58L/h	Antithrombins and Fibrinolytic Agents and Hypoglycemic Agents and Anticoagulants and Hypolipidemic Agents	NA	NA	NA	NA	Heparin cofactor 2,Antithrombin-III	SULODEXIDE	Syntex S.A	Syntex S.A	Antithrombotic and antithrombin activity is of great pharmacologic interest and makes sulodexide a suitable drug for the prophylaxis and treatment of arterial and venous peripheral diseases	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10676	Th1148	Aliskiren	NA	551.7583	C30H53N3O6	NA	NA	>95°C	24 hours	Aliskiren is an anti-hypertensive (blood pressure lowering) medicine. It works by decreasing substances in the body that narrow blood vessels and raise blood pressure. It is chemically, (2S,4S,5S,7S)-5-amino-N-(3-amino-2,2-dimethyl-3-oxopropyl)-4-hydroxy-7-[[4-methoxy-3-(3-methoxypropoxy)phenyl]methyl]-8-methyl-2-propan-2-ylnonanamide.	It is used to treat hypertension, renal impairment and hepatic impairment	Aliskiren shows high specificity for human renin, with almost no inhibitory effect against other aspartic peptidases such as cathepsin D and pepsin. Although aliskiren also exhibits high affinity for primate renin, it is significantly less active against renin from dog, rat, rabbit, pig and cat. This high potency for human renin compensates for the relatively low oral bioavailability of the drug.	Renin inhibitor that inhibits the conversion of angiotensinogen to angiotensin I. The decrease in antiotensin I causes a decrease in angiotensin II, a potent blood pressure elevating peptide.	NA	NA	NA	NA	NA	Renin inhibitor	NA	NA	NA	Cyclosporine, Itraconazole: Avoid concomitant use	Renin	Tekturna	Physicians Total Care, Inc.	Physicians Total Care, Inc.	This medication is used to treat high blood pressure (hypertension). Lowering high blood pressure helps prevent strokes, heart attacks, and kidney problems. Aliskiren works by relaxing blood vessels so blood can flow more easily. It belongs to a class of drugs known as direct renin inhibitors.	(2S,4S,5S,7S)-N-(2-carbamoyl-2-methylpropyl)-5-amino-4-hydroxy-2,7-diisopropyl-8-[4-methoxy-3-(3-methoxypropoxy)phenyl]-octanamide hemifumarate	Tekturna is supplied as a light-pink, biconvex round tablet containing 150Ã‚Â mg of aliskiren, and as a light-red biconvex ovaloid tablet containing 300Ã‚Â mg of aliskiren.Ã‚Â	150Ã‚Â mg light pink biconvex round tablet, imprinted NVR/IL, 300 mg light red biconvex ovaloid round tablet, imprinted NVR/IU	Oral route	The usual recommended starting dose of Tekturna is 150Ã‚Â mg once daily.Ã‚Â In patients whose blood pressure is not adequately controlled, the daily dose may be increased to 300Ã‚Â mg. The antihypertensive effect of a given dose is substantially attained (85-90%) by 2 weeks.	None	Hives; vomiting, severe stomach pain; dizziness, diarrhea, difficult breathing; swelling of your face, lips, tongue, or throat.	Link	NA	NA
10677	Th1148	Aliskiren	NA	551.7583	C30H53N3O6	NA	NA	>95°C	24 hours	Aliskiren is an anti-hypertensive (blood pressure lowering) medicine. It works by decreasing substances in the body that narrow blood vessels and raise blood pressure. It is chemically, (2S,4S,5S,7S)-5-amino-N-(3-amino-2,2-dimethyl-3-oxopropyl)-4-hydroxy-7-[[4-methoxy-3-(3-methoxypropoxy)phenyl]methyl]-8-methyl-2-propan-2-ylnonanamide.	It is used to treat hypertension, renal impairment and hepatic impairment	Aliskiren shows high specificity for human renin, with almost no inhibitory effect against other aspartic peptidases such as cathepsin D and pepsin. Although aliskiren also exhibits high affinity for primate renin, it is significantly less active against renin from dog, rat, rabbit, pig and cat. This high potency for human renin compensates for the relatively low oral bioavailability of the drug.	Renin inhibitor that inhibits the conversion of angiotensinogen to angiotensin I. The decrease in antiotensin I causes a decrease in angiotensin II, a potent blood pressure elevating peptide.	NA	NA	NA	NA	NA	Renin inhibitor	NA	NA	NA	NA	Renin	Tekturna	Novartis Pharmaceuticals Corporation	Novartis Pharmaceuticals Corporation	This medication is used to treat high blood pressure (hypertension). Lowering high blood pressure helps prevent strokes, heart attacks, and kidney problems. Aliskiren works by relaxing blood vessels so blood can flow more easily. It belongs to a class of drugs known as direct renin inhibitors.	(2S,4S,5S,7S)-N-(2-carbamoyl-2-methylpropyl)-5-amino-4-hydroxy-2,7-diisopropyl-8-[4-methoxy-3-(3-methoxypropoxy)phenyl]-octanamide hemifumarate	Tekturna is supplied as a light-pink, biconvex round tablet containing 150Ã‚Â mg of aliskiren, and as a light-red biconvex ovaloid tablet containing 300Ã‚Â mg of aliskiren.Ã‚Â	150Ã‚Â mg light pink biconvex round tablet, imprinted NVR/IL, 300 mg light red biconvex ovaloid round tablet, imprinted NVR/IU	Oral route	The usual recommended starting dose of Tekturna is 150Ã‚Â mg once daily.Ã‚Â In patients whose blood pressure is not adequately controlled, the daily dose may be increased to 300Ã‚Â mg. The antihypertensive effect of a given dose is substantially attained (85-90%) by 2 weeks.	None	Hives; vomiting, severe stomach pain; dizziness, diarrhea, difficult breathing; swelling of your face, lips, tongue, or throat.	Link	NA	NA
10678	Th1148	Aliskiren	NA	551.7583	C30H53N3O6	NA	NA	>95°C	24 hours	Aliskiren is an anti-hypertensive (blood pressure lowering) medicine. It works by decreasing substances in the body that narrow blood vessels and raise blood pressure. It is chemically, (2S,4S,5S,7S)-5-amino-N-(3-amino-2,2-dimethyl-3-oxopropyl)-4-hydroxy-7-[[4-methoxy-3-(3-methoxypropoxy)phenyl]methyl]-8-methyl-2-propan-2-ylnonanamide.	It is used to treat hypertension, renal impairment and hepatic impairment	Aliskiren shows high specificity for human renin, with almost no inhibitory effect against other aspartic peptidases such as cathepsin D and pepsin. Although aliskiren also exhibits high affinity for primate renin, it is significantly less active against renin from dog, rat, rabbit, pig and cat. This high potency for human renin compensates for the relatively low oral bioavailability of the drug.	Renin inhibitor that inhibits the conversion of angiotensinogen to angiotensin I. The decrease in antiotensin I causes a decrease in angiotensin II, a potent blood pressure elevating peptide.	NA	NA	NA	NA	NA	Renin inhibitor	NA	NA	NA	Some products that may interact with this drug include: cisapride, dofetilide, lithium, drugs that may increase the level of potassium in the blood (including ACE inhibitors such as benazepril/lisinopril, ARBs such as candesartan/losartan, birth control pills containing drospirenone).	Renin	Tekturna HCT	Novartis Pharmaceuticals Corporation	Novartis Pharmaceuticals Corporation	This product is used to treat high blood pressure (hypertension). Lowering high blood pressure helps prevent strokes, heart attacks, and kidney problems. This product contains 2 medications: aliskiren and hydrochlorothiazide. Aliskiren works by relaxing blood vessels so blood can flow more easily. It belongs to a class of drugs known as direct renin inhibitors. Hydrochlorothiazide causes your body to get rid of extra salt and water by making more urine. It is called a water pill or diuretic.	NA	TekturnaÃ‚Â HCT is supplied asÃ‚Â biconvex, ovaloid film-coated tablets.	150Ã‚Â mg/12.5Ã‚Â mg tablets: white, biconvex ovaloid, film-coated tablets imprinted with NVR/LCI, 150 mg/25 mg tablets: pale yellow, biconvex ovaloid, film-coated tablets imprinted with NVR/CLL, 300 mg/12.5 mg tablets: violet white, biconvex ovaloid, film-coated tablets imprinted with NVR/CVI, 300 mg/2	Oral route	Ã‚Â Initiate with 12.5 mg/150 mg PO qDay; after 2-4 weeks, may increase dose if needed; not to exceed 25 mg/300 mg	Do not use aliskiren with ARBs or ACEIs in patients with diabetes. Tekturna HCT is contraindicated in patients with anuria or hypersensitivity to sulfonamide derived drugs like HCTZ or to any of the components. Hypersensitivity reactions may range from urticaria to anaphylaxis.	Dizziness or lightheadedness may occur as your body adjusts to the medication. If either of these effects persists or worsens, tell your doctor or pharmacist promptly.	Link	NA	NA
10679	Th1148	Aliskiren	NA	551.7583	C30H53N3O6	NA	NA	>95°C	24 hours	Aliskiren is an anti-hypertensive (blood pressure lowering) medicine. It works by decreasing substances in the body that narrow blood vessels and raise blood pressure. It is chemically, (2S,4S,5S,7S)-5-amino-N-(3-amino-2,2-dimethyl-3-oxopropyl)-4-hydroxy-7-[[4-methoxy-3-(3-methoxypropoxy)phenyl]methyl]-8-methyl-2-propan-2-ylnonanamide.	It is used to treat hypertension, renal impairment and hepatic impairment	Aliskiren shows high specificity for human renin, with almost no inhibitory effect against other aspartic peptidases such as cathepsin D and pepsin. Although aliskiren also exhibits high affinity for primate renin, it is significantly less active against renin from dog, rat, rabbit, pig and cat. This high potency for human renin compensates for the relatively low oral bioavailability of the drug.	Renin inhibitor that inhibits the conversion of angiotensinogen to angiotensin I. The decrease in antiotensin I causes a decrease in angiotensin II, a potent blood pressure elevating peptide.	NA	NA	NA	NA	NA	Renin inhibitor	NA	NA	NA	Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Increased risk of renal impairment and loss of antihypertensive effect, Simvastatin: Avoid doses greater than 20 mg daily. Ã‚Â	Renin	Tekamlo	Novartis Pharmaceuticals Corporation	Novartis Pharmaceuticals Corporation	TekamloÃ‚Â is a combination of aliskiren, a renin inhibitor, and amlodipine, a dihydropyridine calcium channel blocker, indicated for the treatment of hypertension, alone or with other antihypertensive agents, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions.	NA	Tablets (aliskireNAmlodipine): 150 mg/5 mg, 150 mg/10 mg, 300 mg/5 mg, 300 mg/10 mg	150 mg aliskiren/5Ã‚Â mg amlodipine tablets: Non-scored light yellow, ovaloid convex shaped film-coated tablet with a beveled edgeÃ‚Â with debossing Ã¢â‚¬Å“T2Ã¢â‚¬Â on one side and Ã¢â‚¬Å“NVRÃ¢â‚¬Â on the reverse side of the tablet, 150 mg aliskiren/10 mg amlodipine tablets: Non-scored yellow, ovaloid convex shaped f	Oral route	The recommended initial once-daily dose of Tekamlo is 150 mg/5 mg. Titrate as needed to a maximum of 300 mg/10 mg. The blood pressure lowering effects are largely attained within 1 to 2 weeks. If blood pressure remains uncontrolled after 2 to 4 weeks of therapy, titrate the dose to a maximum of Tekamlo 300 mg/10 mg once daily.	Do not use with angiotensin receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors (ACEIs) in patients with diabetes. Known hypersensitivity to any of the components.	Swelling of lower legs, diarrhea,dizziness, cough, flu-like symptoms, tiredness, high levels of potassium in the blood (hyperkalemia)	Link	NA	NA
10680	Th1148	Aliskiren	NA	551.7583	C30H53N3O6	NA	NA	>95°C	24 hours	Aliskiren is an anti-hypertensive (blood pressure lowering) medicine. It works by decreasing substances in the body that narrow blood vessels and raise blood pressure. It is chemically, (2S,4S,5S,7S)-5-amino-N-(3-amino-2,2-dimethyl-3-oxopropyl)-4-hydroxy-7-[[4-methoxy-3-(3-methoxypropoxy)phenyl]methyl]-8-methyl-2-propan-2-ylnonanamide.	It is used to treat hypertension, renal impairment and hepatic impairment	Aliskiren shows high specificity for human renin, with almost no inhibitory effect against other aspartic peptidases such as cathepsin D and pepsin. Although aliskiren also exhibits high affinity for primate renin, it is significantly less active against renin from dog, rat, rabbit, pig and cat. This high potency for human renin compensates for the relatively low oral bioavailability of the drug.	Renin inhibitor that inhibits the conversion of angiotensinogen to angiotensin I. The decrease in antiotensin I causes a decrease in angiotensin II, a potent blood pressure elevating peptide.	NA	NA	NA	NA	NA	Renin inhibitor	NA	NA	NA	Antidiabetic Drugs: Antidiabetic dosage adjustment may be required	Renin	Amturnide	Novartis Pharmaceuticals Corporation	Novartis Pharmaceuticals Corporation	Amturnide is indicated for the treatment of hypertension, to lower blood pressure. Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions.Ã‚Â	NA	Tablets (aliskiren/ amlodipine/ HCTZ): 150/5/12.5,Ã‚Â 300/5/12.5,Ã‚Â 300/5/25, 300/10/12.5, 300/10/25 mg.Ã‚Â	Tablets are convex ovaloid with a beveled edge, film-coated, and unscored.	Oral route	Dose once-daily.Ã‚Â The dosage may be increased after 2Ã‚Â weeks of therapy.Ã‚Â The maximum recommended dose of Amturnide is 300/10/25 mg. High-fat meals decrease absorption of aliskiren substantially.	Do not use with angiotensin receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors (ACEIs) in patients with diabetes, Anuria, Hypersensitivity to sulfonamide derived drugs or to any of the components.	Dizziness or lightheadedness as your body adjusts to the medication. Swelling hands/ankles/feet, flushing, headache, or diarrhea may also occur.	Link	NA	NA
10681	Th1149	Ragweed Pollen Extract	NA	NA	NA	NA	NA	NA	NA	Ragweed pollen extract has been developed by Curalogic. The company has initiated a phaseÃ‚Â IIIÃ‚Â trial with its product for oral immunotherapy of ragweed allergy. While traditional disease-modifying immunotherapeutics are administered by subcutaneous injection, Curalogic has developed a more convenient orally administered drug.	Investigated for use/treatment in allergic reaction.	Precise mechanism of allergen immunotherapy is not known	Ragweed pollen extract is the oral immunotherapy delivered via microencapsulated beads put into a capsule, which enables the antigen to be delivered more efficiently to the Peyer's patches in the jejunum and duodenum, where the antigen can be presented and processed and not destroyed by stomach acid.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	Ragwitek	Merck Sharp & Dohme	Merck Sharp & Dohme	Ragwitek is anÃ‚Â allergenÃ‚Â extract indicated asÃ‚Â immunotherapyÃ‚Â for the treatment of shortÃ‚Â ragweedÃ‚Â pollen-induced allergicÃ‚Â rhinitis, with or withoutconjunctivitis, confirmed by positive skin test or in vitro testing for pollen-specificÃ‚Â IgEÃ‚Â antibodies for short ragweed pollen. Ragwitek is approved for use in adults 18 through 65 years of age.	NA	NA	Tablets	Oral route	One ragwitek tablet daily.	Ragwitek is contraindicated in patients with severe, unstable or uncontrolled asthma, history of any severe systemic allergic reaction, history of any severe local reaction after taking any sublingual allergen immunotherapy, history of eosinophilic esophagitis and hypersensitivity to any of the inactive ingredients [gelatin, mannitol, and sodium hydroxide] contained in this product.	Throat irritation, oralpruritus, ear pruritus, oralÃ‚Â paraesthesia, mouth edema, and tongue pruritus.	Link	NA	NA
10711	Th1164	Antithrombin Alfa	NA	57,215	C2191H3451N583O656S18	NA	NA	NA	11.6 (84.7) for 50 IU/KG to17.7 (60.9) for 100IU/KG	Antithrombin (Recombinant) and plasma-derived antithrombin both contain six cysteine residues forming three disulphide bridges and 3-4 N-linked carbohydrate moieties. The glycosylation profile of antithrombin (Recombinant) is different from plasma-derived antithrombin, which results in an increased heparin affinity. When assayed in the presence of excess of heparin the potency of the recombinant product is not different from that of plasma-derived product.	Indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients	Hereditary AT deficiency causes an increased risk of venous thromboembolism (VTE). During high-risk situations such as surgery or trauma or for pregnant women, during the peripartum period, the risk of development of VTEs as compared to the normal population in these situations is increased by a factor 10 to 506,7. In hereditary antithrombin deficient patients ATryn restores (normalizes) plasma AT activity levels during peri-operative and peri-partum periods.	Antithrombin (AT) plays a central role in the regulation of hemostasis. AT is the principal inhibitor of thrombin and Factor Xa5, the serine proteases that play pivotal roles in blood coagulation. AT neutralizes the activity of thrombin and Factor Xa by forming a complex which is rapidly removed from the circulation. The ability of antithrombin to inhibit thrombin and Factor Xa can be enhanced by greater than 300 to 1000 fold when AT is bound to heparin.	Highest dose tested was 360mg/kg/day in rats resulted in transient limb swelling.	Not metabolized.	Given IV so not absorbed.	Dose of: 50IU/kg: 126.2 ml/kg 100IU/kg: 156.1 ml/kg Vd in hereditary deficient pregnant women in high risk situations had increased Vd of 14.3L.	Dose of: 50IU/kg: 9.6 ml/hr/kg 100IU/kg: 7.2 ml/hr/kg Cl in hereditary deficient pregnant women in high risk situations had increased Cl of 1.38L/h.	Anticoagulants,Decreased Coagulation Factor Activity,Factor Xa Inhibitors,Recombinant Antithrombin,Thrombin Inhibitors	NA	NA	NA	NA	Prothrombin,Coagulation factor X	NA	NA	NA	NA	NA	NA	NA	NA	The dosage is to be individualized based on the patient's pre-treatment functional AT activity level (expressed in percent of normal) and body weight (expressed in kilograms) and using therapeutic drug monitoring	NA	Hemorrhage (intra-abdominal, hemarthrosis and post procedural)	Link	NA	NA
10712	Th1164	Antithrombin Alfa	NA	57,215	C2191H3451N583O656S19	NA	NA	NA	11.6 (84.7) for 50 IU/KG to17.7 (60.9) for 100IU/KG	Antithrombin (Recombinant) and plasma-derived antithrombin both contain six cysteine residues forming three disulphide bridges and 3-4 N-linked carbohydrate moieties. The glycosylation profile of antithrombin (Recombinant) is different from plasma-derived antithrombin, which results in an increased heparin affinity. When assayed in the presence of excess of heparin the potency of the recombinant product is not different from that of plasma-derived product.	Indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients	Hereditary AT deficiency causes an increased risk of venous thromboembolism (VTE). During high-risk situations such as surgery or trauma or for pregnant women, during the peripartum period, the risk of development of VTEs as compared to the normal population in these situations is increased by a factor 10 to 506,7. In hereditary antithrombin deficient patients ATryn restores (normalizes) plasma AT activity levels during peri-operative and peri-partum periods.	Antithrombin (AT) plays a central role in the regulation of hemostasis. AT is the principal inhibitor of thrombin and Factor Xa5, the serine proteases that play pivotal roles in blood coagulation. AT neutralizes the activity of thrombin and Factor Xa by forming a complex which is rapidly removed from the circulation. The ability of antithrombin to inhibit thrombin and Factor Xa can be enhanced by greater than 300 to 1000 fold when AT is bound to heparin.	Highest dose tested was 360mg/kg/day in rats resulted in transient limb swelling.	Not metabolized.	Given IV so not absorbed.	Dose of: 50IU/kg: 126.2 ml/kg 100IU/kg: 156.1 ml/kg Vd in hereditary deficient pregnant women in high risk situations had increased Vd of 14.3L.	Dose of: 50IU/kg: 9.6 ml/hr/kg 100IU/kg: 7.2 ml/hr/kg Cl in hereditary deficient pregnant women in high risk situations had increased Cl of 1.38L/h.	Anticoagulants,Decreased Coagulation Factor Activity,Factor Xa Inhibitors,Recombinant Antithrombin,Thrombin Inhibitors	NA	NA	NA	NA	Prothrombin,Coagulation factor X	Atryn	Gtc Biotherapeutics, Inc.	Gtc Biotherapeutics, Inc.	It is indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients	NA	1750 [iU]/1	injection, powder, lyophilized, for solution	IV	The dosage is to be individualized based on the patient's pre-treatment functional AT activity level (expressed in percent of normal) and body weight (expressed in kilograms) and using therapeutic drug monitoring	NA	Hemorrhage (intra-abdominal, hemarthrosis and post procedural)	Link	NA	NA
10713	Th1164	Antithrombin Alfa	NA	57,215	C2191H3451N583O656S20	NA	NA	NA	11.6 (84.7) for 50 IU/KG to17.7 (60.9) for 100IU/KG	Antithrombin (Recombinant) and plasma-derived antithrombin both contain six cysteine residues forming three disulphide bridges and 3-4 N-linked carbohydrate moieties. The glycosylation profile of antithrombin (Recombinant) is different from plasma-derived antithrombin, which results in an increased heparin affinity. When assayed in the presence of excess of heparin the potency of the recombinant product is not different from that of plasma-derived product.	Indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients	Hereditary AT deficiency causes an increased risk of venous thromboembolism (VTE). During high-risk situations such as surgery or trauma or for pregnant women, during the peripartum period, the risk of development of VTEs as compared to the normal population in these situations is increased by a factor 10 to 506,7. In hereditary antithrombin deficient patients ATryn restores (normalizes) plasma AT activity levels during peri-operative and peri-partum periods.	Antithrombin (AT) plays a central role in the regulation of hemostasis. AT is the principal inhibitor of thrombin and Factor Xa5, the serine proteases that play pivotal roles in blood coagulation. AT neutralizes the activity of thrombin and Factor Xa by forming a complex which is rapidly removed from the circulation. The ability of antithrombin to inhibit thrombin and Factor Xa can be enhanced by greater than 300 to 1000 fold when AT is bound to heparin.	Highest dose tested was 360mg/kg/day in rats resulted in transient limb swelling.	Not metabolized.	Given IV so not absorbed.	Dose of: 50IU/kg: 126.2 ml/kg 100IU/kg: 156.1 ml/kg Vd in hereditary deficient pregnant women in high risk situations had increased Vd of 14.3L.	Dose of: 50IU/kg: 9.6 ml/hr/kg 100IU/kg: 7.2 ml/hr/kg Cl in hereditary deficient pregnant women in high risk situations had increased Cl of 1.38L/h.	Anticoagulants,Decreased Coagulation Factor Activity,Factor Xa Inhibitors,Recombinant Antithrombin,Thrombin Inhibitors	NA	NA	NA	NA	Prothrombin,Coagulation factor X	Atryn	R Evo Bioloigics, Inc.	R Evo Bioloigics, Inc.	It is indicated for the prevention of peri-operative and peri-partum thromboembolic events in hereditary antithrombin deficient patients	NA	525 [iU]/mL	injection, powder, lyophilized, for solution	IV	The dosage is to be individualized based on the patient's pre-treatment functional AT activity level (expressed in percent of normal) and body weight (expressed in kilograms) and using therapeutic drug monitoring	NA	Hemorrhage (intra-abdominal, hemarthrosis and post procedural)	Link	NA	NA
10714	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	Enhanced anticoagulant effect; increased risk of bleeding complications with Heparin; Heparin also Decreases half-life of antithrombin III	Antithrombin-III	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	Link	NA	NA
10715	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE IIIÃ‚Â® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III.	Antithrombin-III	Thrombate III	GRIFOLS USA, LLC	GRIFOLS USA, LLC	Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism.	NA	NA	kit	NA	Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%.	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	NA	NA	NA
10716	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE IIIÃ‚Â® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III.	Antithrombin-III	Thrombate III	Grifols Therapeutics Inc	Grifols Therapeutics Inc	Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism.	NA	500 unit	powder for solution	NA	Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%.	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	NA	NA	NA
10717	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE IIIÃ‚Â® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III.	Antithrombin-III	Thrombate III	Grifols Therapeutics Inc	Grifols Therapeutics Inc	Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism.	NA	1000 unit	powder for solution	NA	Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%.	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	NA	NA	NA
10718	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE IIIÃ‚Â® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III.	Antithrombin-III	Thrombate III	GRIFOLS USA, LLC	GRIFOLS USA, LLC	Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism.	NA	NA	kit	NA	Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%.	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	NA	NA	NA
10719	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE IIIÃ‚Â® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III.	Antithrombin-III	Thrombate III Pws IV 1000iu/vial	Miles Inc. Pharmaceutical Division	Miles Inc. Pharmaceutical Division	Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism.	NA	1000 unit	powder for solution	NA	Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%.	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	NA	NA	NA
10720	Th1165	Antithrombin III human	NA	58000	NA	NA	NA	NA	2.5 - 3.8 hs	A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily.	Short-term replacement therapy for prevention or treatment of thromboembolism in selected patients with congenital antithrombin III deficiency at high risk for thromboembolism (i.e., those undergoing surgical or obstetrical procedures) or those with thromboembolism	It s the major plasma inhibitor of thrombin. Inactivation of thrombin by AT-III occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT-III. AT-III is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin.	Neutralizes serine proteinases such as thrombin, plasmin, and activated coagulation factors IX, X, XI, and XII; Principally neutralizes thrombin and activated coagulation factor X (Xa); Neutralization of factor Xa prevents thrombin generation (e.g., decreased formation of prothrombin fragment 1.2 [F1 and F2]); Neutralization of thrombin prevents conversion of fibrinogen to fibrin; lowly and irreversibly complexes stoichiometrically with these coagulation factors; such reactions are rapid in presence of endogenous heparin-like proteoglycans or exogenous heparin; Inhibits thrombus formation.	NA	<5% metabolized to low molecular weight breakdown products.	Therapeutic target plasma concentrations in patients with congenital antithrombin III deficiency range from 80–120% of values in healthy adults. At plasma concentrations =70% of normal, increased thrombin generation. Supraphysiologic plasma concentrations (e.g., 150–200% of normal) have increased bleeding risk in patients with sepsis and disseminated intravascular coagulation, not known whether supraphysiologic concentrations increase bleeding risk in patients with congenital antithrombin III deficiency.	Distributed into plasma (39%), extravascular space (49%), and vascular endothelial cells (11%).	NA	Alpha-Globulins,Amino Acids, Peptides, and Proteins,Anticoagulants,Antithrombin III,Antithrombin III, agonists,Antithrombin Proteins,Biological Factors,Blood and Blood Forming Organs,Blood Coagulation Factor Inhibitors,Blood Proteins,Carbohydrates,Drugs that are Mainly Renally Excreted,Enzyme Inhibitors,Globulins,Glycosaminoglycans,Hematologic Agents,Oligosaccharides,Peptides,Polysaccharides,Proteins,Serum Globulins	NA	NA	NA	The anticoagulant effect of heparin is enhanced by concurrent treatment with Antithrombin III (Human), THROMBATE IIIÃ‚Â® (antithrombin) in patients with hereditary AT-III deficiency. Thus, in order to avoid bleeding, reduced dosage of heparin is recommended during treatment with THROMBATE (antithrombin) III.	Antithrombin-III	Thrombate III Pws IV 500iu/vial	Miles Inc. Pharmaceutical Division	Miles Inc. Pharmaceutical Division	Indicated for the treatment of patients with hereditary antithrombin III deficiency in connection with surgical or obstetrical procedures or when they suffer from thromboembolism.	NA	500 unit	powder for solution	NA	Dosage should be determined on an individual basis based on the pre-therapy plasma antithrombin III (AT-III) level, in order to increase plasma AT-III levels to the level found in normal human plasma (100%). It is recommended that following an initial dose of THROMBATE (antithrombin) III, plasma levels of AT-III be initially monitored at least every 12 hours and before the next infusion of THROMBATE (antithrombin) III to maintain plasma AT-III levels greater than 80%.	NA	Dizziness, chest tightness, nausea, foul taste, chills, cramps, shortness of breath, chest pain, film over eye, lightheadedness, bowel fullness, hives, fever, oozing, hematoma formation.	NA	NA	NA
10732	Th1168	Autologous cultured chondrocytes	NA	NA	NA	NA	NA	NA	NA	Autologous cultured chondrocytes, the Carticel product, are derived from in vitro expansion of chondrocytes harvested from the patient's normal, femoral articular cartilage. Biopsies from a lesser-weight bearing area are the credit of chondrocytes, which are isolated, expanded through cell culture, and implanted into articular cartilage defects beneath an autologous periosteal flap. Prior to final packaging, cell viability is assessed to be at least 80%.	Is indicated for the repair of symptomatic cartilage defects of the femoral condyle (medial, lateral or trochlea), caused by acute or repetitive trauma, in patients who have had an inadequate response to a prior arthroscopic or other surgical repair procedure (e.g., debridement, microfracture, drilling/abrasion arthroplasty, or osteochondral allograft/autograft).	Published data show that autologous chondrocyte implantation (ACI) is more likely than MST to result in hyaline-like cartilage at the repair site.1,2,4,5 However, because of differences in study design, lesion size and concomitant patient conditions, these data are not sufficient to draw conclusions concerning the long-term correlation of histology and clinical outcomes.	Hyaline cartilage forms the articular surface of the femoral condyle. Studies have shown that implantation of autologous chondrocytes into the articular defect can result in the development of hyaline-like cartilage	Unwanted effects from therapy include arthrofibrosis/joint adhesions, graft overgrowth, chondromalacia or chondrosis, cartilage injury, graft complication, meniscal lesion and graft delamination in less than 5% of total patients who underwent treatment.	NA	NA	NA	NA	Autologous Cultured Cell	NA	NA	NA	NA	NA	Carticel	Genzyme Corporation	Genzyme Corporation	NA	NA	Strength: 12000000 1/1	Implant	Intra-auricular	NA	Carticel should not be used in patients with a known history of hypersensitivity to gentamicin, other aminoglycosides or materials of bovine origin. Gentamicin is added to both the cartilage biopsy transport media and in the culture media used during the processing of Carticel. Residual quantities of gentamicin up to 5 ÃŽÂ¼g/mL are present in the Carticel product. Fetal bovine serum is a component in the culture medium used to propagate the autologous chondrocytes. Trace quantities of bovine-derived proteins may be present in the Carticel product.	The most common serious adverse events (> 5% of patients) derived from the STAR study include arthrofibrosis/ joint adhesion, graft overgrowth, chondromalacia or chondrosis, cartilage injury, graft complication, meniscal lesion and graft delamination. Only serious adverse events were collected in this study.	Link	NA	NA
10733	Th1169	Beractant	NA	NA	NA	NA	NA	NA	20Ã¢â‚¬â€œ30 h.	Beractant is a pulmonary surfactant made from natural bovine lung extract.	Beractant is indicated for Respiratory Distress Syndrome (RDS) in premature infants.	Endogenous pulmonary surfactant lowers surface tension on alveolar surfaces during respiration and stabilizes the alveoli against collapse at resting transpulmonary pressures. Deficiency of pulmonary surfactant causes Respiratory Distress Syndrome (RDS) in premature infants. SURVANTA replenishes surfactant and restores surface activity to the lungs of these infants.	It reproducibly lowers minimum surface tension to less than 8 dynes/cm as measured by the pulsating bubble surfactometer and Wilhelmy Surface Balance.	NA	In surfactant-deficient premature rabbits and lambs, alveolar clearance of radio-labelled lipid components of beractant is rapid. Most of the dose becomes lung-associated within hours of administration, and the lipids enter endogenous surfactant pathways of reutilization and recycling. Limited animal experiments have not found effects of beractant on endogenous surfactant metabolism.	Beractant is administered directly to the target organ, the lungs, where biophysical effects occur at the alveolar surface.	NA	NA	Alveolar Surface Tension Reduction,Bradycardia-Causing Agents,Complex Mixtures,Pulmonary Surfactants,Respiratory System Agents,Surface-Active Agents,Surfactant Activity	NA	NA	NA	Bretylium may increase the bradycardic activities of Beractant; Beractant may increase the bradycardic activities of Ceritinib; Esmolol may increase the bradycardic activities of Beractant; Beractant may increase the bradycardic activities of Ivabradine; Beractant may increase the atrioventricular blocking (AV block) activities of Lacosamide; Octreotide may increase the bradycardic activities of Beractant; Ruxolitinib may increase the bradycardic activities of Beractant; Tofacitinib may increase the bradycardic activities of Beractant.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	pale skin; slow heartbeat; breathing that stops; urinating less than usual; or blood in the urine; noisy breathing; feeding or bowel problems; or bleeding around the endotracheal tube.	Link	NA	NA
10734	Th1169	Beractant	NA	NA	NA	NA	NA	NA	20Ã¢â‚¬â€œ30 h.	Beractant is a pulmonary surfactant made from natural bovine lung extract.	Beractant is indicated for Respiratory Distress Syndrome (RDS) in premature infants.	Endogenous pulmonary surfactant lowers surface tension on alveolar surfaces during respiration and stabilizes the alveoli against collapse at resting transpulmonary pressures. Deficiency of pulmonary surfactant causes Respiratory Distress Syndrome (RDS) in premature infants. SURVANTA replenishes surfactant and restores surface activity to the lungs of these infants.	In vitro, SURVANTA reproducibly lowers minimum surface tension to less than 8 dynes/cm as measured by the pulsating bubble surfactometer and Wilhelmy Surface Balance. In situ, SURVANTA restores pulmonary compliance to excised rat lungs artificially made surfactantdeficient. In vivo, single SURVANTA doses improve lung pressure-volume measurements, lung compliance, and oxygenation in premature rabbits and sheep.	NA	In surfactant-deficient premature rabbits and lambs, alveolar clearance of radio-labelled lipid components of beractant is rapid. Most of the dose becomes lung-associated within hours of administration, and the lipids enter endogenous surfactant pathways of reutilization and recycling. Limited animal experiments have not found effects of beractant on endogenous surfactant metabolism.	Beractant is administered directly to the target organ, the lungs, where biophysical effects occur at the alveolar surface.	NA	NA	Alveolar Surface Tension Reduction,Bradycardia-Causing Agents,Complex Mixtures,Pulmonary Surfactants,Respiratory System Agents,Surface-Active Agents,Surfactant Activity	NA	NA	NA	Bretylium may increase the bradycardic activities of Beractant; Beractant may increase the bradycardic activities of Ceritinib; Esmolol may increase the bradycardic activities of Beractant; Beractant may increase the bradycardic activities of Ivabradine; Beractant may increase the atrioventricular blocking (AV block) activities of Lacosamide; Octreotide may increase the bradycardic activities of Beractant; Ruxolitinib may increase the bradycardic activities of Beractant; Tofacitinib may increase the bradycardic activities of Beractant.	NA	Survanta	Abb Vie Inc.	Abb Vie Inc.	SURVANTA is indicated for prevention and treatment (Ã¢â‚¬Å“rescueÃ¢â‚¬Â) of Respiratory Distress Syndrome (RDS) (hyaline membrane disease) in premature infants. SURVANTA significantly reduces the incidence of RDS, mortality due to RDS and air leak complications.	NA	25 mg/mL	Suspension	endotracheal	Each dose of SURVANTA is 100 mg of phospholipids/kg birth weight (4 mL/kg).	NA	pale skin; slow heartbeat; breathing that stops; urinating less than usual; or blood in the urine; noisy breathing; feeding or bowel problems; or bleeding around the endotracheal tube.	NA	NA	NA
10735	Th1169	Beractant	NA	NA	NA	NA	NA	NA	20Ã¢â‚¬â€œ30 h.	Beractant is a pulmonary surfactant made from natural bovine lung extract.	Beractant is indicated for Respiratory Distress Syndrome (RDS) in premature infants.	Endogenous pulmonary surfactant lowers surface tension on alveolar surfaces during respiration and stabilizes the alveoli against collapse at resting transpulmonary pressures. Deficiency of pulmonary surfactant causes Respiratory Distress Syndrome (RDS) in premature infants. SURVANTA replenishes surfactant and restores surface activity to the lungs of these infants.	In vitro, SURVANTA reproducibly lowers minimum surface tension to less than 8 dynes/cm as measured by the pulsating bubble surfactometer and Wilhelmy Surface Balance. In situ, SURVANTA restores pulmonary compliance to excised rat lungs artificially made surfactantdeficient. In vivo, single SURVANTA doses improve lung pressure-volume measurements, lung compliance, and oxygenation in premature rabbits and sheep.	NA	In surfactant-deficient premature rabbits and lambs, alveolar clearance of radio-labelled lipid components of beractant is rapid. Most of the dose becomes lung-associated within hours of administration, and the lipids enter endogenous surfactant pathways of reutilization and recycling. Limited animal experiments have not found effects of beractant on endogenous surfactant metabolism.	Beractant is administered directly to the target organ, the lungs, where biophysical effects occur at the alveolar surface.	NA	NA	Alveolar Surface Tension Reduction,Bradycardia-Causing Agents,Complex Mixtures,Pulmonary Surfactants,Respiratory System Agents,Surface-Active Agents,Surfactant Activity	NA	NA	NA	Bretylium may increase the bradycardic activities of Beractant; Beractant may increase the bradycardic activities of Ceritinib; Esmolol may increase the bradycardic activities of Beractant; Beractant may increase the bradycardic activities of Ivabradine; Beractant may increase the atrioventricular blocking (AV block) activities of Lacosamide; Octreotide may increase the bradycardic activities of Beractant; Ruxolitinib may increase the bradycardic activities of Beractant; Tofacitinib may increase the bradycardic activities of Beractant.	NA	Survanta	Abbvie Corporation	Abbvie Corporation	SURVANTA is indicated for prevention and treatment (Ã¢â‚¬Å“rescueÃ¢â‚¬Â) of Respiratory Distress Syndrome (RDS) (hyaline membrane disease) in premature infants. SURVANTA significantly reduces the incidence of RDS, mortality due to RDS and air leak complications.	NA	25 mg	Suspension	intratracheal	Each dose of SURVANTA is 100 mg of phospholipids/kg birth weight (4 mL/kg).	NA	pale skin; slow heartbeat; breathing that stops; urinating less than usual; or blood in the urine; noisy breathing; feeding or bowel problems; or bleeding around the endotracheal tube.	NA	NA	NA
10742	Th1171	C1 Esterase Inhibitor (Human)	NA	68000	NA	NA	NA	NA	Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours	Recombinant human C1 esterase inhibitor is a human protein developed through PharmingÃ¢â‚¬â„¢s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated.	For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE).	In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration.	C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity.	NA	NA	NA	NA	NA	NA	NA	NA	NA	Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human).	Plasma protease C1 inhibitor	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA
10743	Th1171	C1 Esterase Inhibitor (Human)	NA	68000	NA	NA	NA	NA	Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours	Recombinant human C1 esterase inhibitor is a human protein developed through PharmingÃ¢â‚¬â„¢s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated.	For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE).	In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration.	C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity.	NA	NA	NA	NA	NA	NA	NA	NA	NA	Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human).	Plasma protease C1 inhibitor	Berinert 1500	Csl Behring Canada Inc	Csl Behring Canada Inc	Berinert is a plasma-derived concentrate of C1 Esterase Inhibitor (Human) indicated for the treatment of acute abdominal, facial, or laryngeal attacks of hereditary angioedema (HAE) in adult and adolescent patients.	NA	1500 unit	kit; powder for solution	IV	Administer Berinert at a dose of 20 International Units (IU) per kg body weight by intravenous injection. Doses lower than 20 IU/kg body weight should not be administered. Berinert is provided as a freeze-dried powder for reconstitution with the Sterile Water for Injection, USP provided. Store the vial in the original carton in order to protect from light. Do not freeze.	Berinert is contraindicated in individuals who have experienced life-threatening hypersensitivity reactions, including anaphylaxis, to C1 esterase inhibitor preparations.	The most serious adverse reaction reported in subjects enrolled in clinical studies who received Berinert was an increase in the severity of pain associated with HAE. The most common adverse reaction reported in greater than 4% of the subjects and greater than placebo among subjects who received Berinert in the placebo-controlled clinical trial was dysgeusia.	Link	NA	NA
10744	Th1171	C1 Esterase Inhibitor (Human)	NA	68000	NA	NA	NA	NA	Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours	Recombinant human C1 esterase inhibitor is a human protein developed through PharmingÃ¢â‚¬â„¢s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated.	For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE).	In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration.	C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity.	NA	NA	NA	NA	NA	NA	NA	NA	NA	Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human).	Plasma protease C1 inhibitor	Berinert 500	Csl Behring Canada Inc	Csl Behring Canada Inc	Berinert is a plasma-derived concentrate of C1 Esterase Inhibitor (Human) indicated for the treatment of acute abdominal, facial, or laryngeal attacks of hereditary angioedema (HAE) in adult and adolescent patients.	NA	500 unit	kit; powder for solution	IV	Administer Berinert at a dose of 20 International Units (IU) per kg body weight by intravenous injection. Doses lower than 20 IU/kg body weight should not be administered. Berinert is provided as a freeze-dried powder for reconstitution with the Sterile Water for Injection, USP provided. Store the vial in the original carton in order to protect from light. Do not freeze.	Berinert is contraindicated in individuals who have experienced life-threatening hypersensitivity reactions, including anaphylaxis, to C1 esterase inhibitor preparations.	The most serious adverse reaction reported in subjects enrolled in clinical studies who received Berinert was an increase in the severity of pain associated with HAE. The most common adverse reaction reported in greater than 4% of the subjects and greater than placebo among subjects who received Berinert in the placebo-controlled clinical trial was dysgeusia.	Link	NA	NA
10745	Th1171	C1 Esterase Inhibitor (Human)	NA	68000	NA	NA	NA	NA	Following intravenous administration of a single dose, the half-life was 56 ± 36 hours.3 Subcutaneous administration produces a half-life of 199.6 hours	Recombinant human C1 esterase inhibitor is a human protein developed through PharmingÃ¢â‚¬â„¢s proprietary technology where the human protein is expressed in milk of transgenic rabbits. Hereditary Angioedema (HAE) is a human genetic disorder caused by a shortage of C1 inhibitor activity and results in an overreaction of the immune system. The disease is characterized by acute attacks of painful and in some cases fatal swelling of several soft tissues (edema), which may last up to five days when untreated.	For routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE).	In clinical studies, intravenous administration demonstrated an increase in plasma levels of C1 inhibitor within approximately one hour or less of administration.	C1 inhibitor is a normal constituent of human blood and is one of the serine proteinase inhibitors (serpins). The primary function of C1 inhibitor is to regulate the activation of the complement and intrinsic coagulation (contact system) pathway. C1 inhibitor also regulates the fibrinolytic system. Regulation of these systems is performed through the formation of complexes between the proteinases and the inhibitor, resulting in inactivation of both and consumption of the C1 inhibitor. HAE patients have low levels of endogenous or functional C1 inhibitor. Although the events that induce attacks of angioedema in HAE patients are not well defined, it is thought by some that increased vascular permeability and the clinical manifestation of HAE attacks are primarily mediated through contact system activation. Suppression of contact system activation by C1 inhibitor through the inactivation of plasma kallikrein and factor XIIa is thought to modulate this vascular permeability by preventing the generation of bradykinin1. Administration of C1 Esterase Inhibitor increases plasma levels of C1 inhibitor activity.	NA	NA	NA	NA	NA	NA	NA	NA	NA	Cyproterone acetate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Danazol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Desogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Dienogest may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Drospirenone may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Estropipate may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethinyl Estradiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Ethynodiol may increase the thrombogenic activities of C1 Esterase Inhibitor (Human); Etonogestrel may increase the thrombogenic activities of C1 Esterase Inhibitor (Human).	Plasma protease C1 inhibitor	Cinryze	Viropharma Biologics Inc	Viropharma Biologics Inc	CINRYZE is a C1 esterase inhibitor indicated for routine prophylaxis against angioedema attacks in adolescent and adult patients with Hereditary Angioedema (HAE).	NA	500 unit	powder for solution	IV	A dose of 1,000 Units CINRYZE can be administered every 3 or 4 days for routine prophylaxis against angioedema attacks in HAE patients. CINRYZE is administered at an injection rate of 1 mL per minute.	CINRYZE is contraindicated in patients who have manifested life-threatening immediate hypersensitivity reactions, including anaphylaxis to the product.	The only serious adverse reaction observed in clinical studies of CINRYZE was cerebrovascular accident. The most common adverse reactions observed were headache, nausea, rash, and vomiting.	Link	NA	NA
10749	Th1173	Conestat alfa	NA	67000	NA	NA	NA	NA	2.4 to 2.7 hours	Conestat alfa is a recombinant, human C1-inhibitor (rhC1INH), for the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. Conestat alfa was approved in October 2010 in all 27 EU member states plus Norway, Iceland and Liechtenstein.	For the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults.	The complement component (protein) C4 is a substrate for activated C1. Patients with HAE have low levels of C4 in the circulation; RUCONEST shows a dose-dependent restoration of complement homeostasis of C4 in HAE patients. A dose of 50 IU/kg of RUCONEST increases plasma C1INH activity levels to greater than 0.7 IU/mL (the lower limit of normal) in HAE patients.	C1INH exerts its inhibitory effect by irreversibly binding several proteases (target proteases) of the contact and complement systems. The effect of RUCONEST on the following target proteases was assessed in vitro: activated C1s, kallikrein, factor XIIa and factor XIa. Inhibition kinetics were found to be comparable with those observed for plasma-derived human C1INH.	The common adverse reactions (= 2%) reported in clinical trials were headache, nausea, and diarrhea. Serious arterial and venous thromboembolic (TE) events have been reported at the recommended dose of plasma derived C1 esterase inhibitor products in patients with risk factors. Risk factors may include the presence of an indwelling venous catheter/access device, prior history of thrombosis, underlying atherosclerosis, use of oral contraceptives or certain androgens, morbid obesity, and immobility. Monitor patients with known risk factors for TE events during and after administration.	NA	Mean Cmax was found to be 1.2 U/mL and Tmax was 0.31 ± 0.10 hr following administration of 50 U/kg.	NA	Clearance was found to be 1207 ± 414 mL/hr following administration of 50 U/kg.	NA	NA	NA	NA	NA	Complement C1r subcomponent,Complement C1s subcomponent,Plasma kallikrein,Coagulation factor XII,Prothrombin,Coagulation factor XI,Tissue-type plasminogen activator	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10750	Th1173	Conestat alfa	NA	67000	NA	NA	NA	NA	2.4 to 2.7 hours	Conestat alfa is a recombinant, human C1-inhibitor (rhC1INH), for the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. Conestat alfa was approved in October 2010 in all 27 EU member states plus Norway, Iceland and Liechtenstein.	For the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults.	The complement component (protein) C4 is a substrate for activated C1. Patients with HAE have low levels of C4 in the circulation; RUCONEST shows a dose-dependent restoration of complement homeostasis of C4 in HAE patients. A dose of 50 IU/kg of RUCONEST increases plasma C1INH activity levels to greater than 0.7 IU/mL (the lower limit of normal) in HAE patients.	C1INH exerts its inhibitory effect by irreversibly binding several proteases (target proteases) of the contact and complement systems. The effect of RUCONEST on the following target proteases was assessed in vitro: activated C1s, kallikrein, factor XIIa and factor XIa. Inhibition kinetics were found to be comparable with those observed for plasma-derived human C1INH.	The common adverse reactions (= 2%) reported in clinical trials were headache, nausea, and diarrhea. Serious arterial and venous thromboembolic (TE) events have been reported at the recommended dose of plasma derived C1 esterase inhibitor products in patients with risk factors. Risk factors may include the presence of an indwelling venous catheter/access device, prior history of thrombosis, underlying atherosclerosis, use of oral contraceptives or certain androgens, morbid obesity, and immobility. Monitor patients with known risk factors for TE events during and after administration.	NA	Mean Cmax was found to be 1.2 U/mL and Tmax was 0.31 ± 0.10 hr following administration of 50 U/kg.	NA	Clearance was found to be 1207 ± 414 mL/hr following administration of 50 U/kg.	NA	NA	NA	NA	NA	Complement C1r subcomponent,Complement C1s subcomponent,Plasma kallikrein,Coagulation factor XII,Prothrombin,Coagulation factor XI,Tissue-type plasminogen activator	Ruconest	Pharming; Santarus, Inc.	Pharming; Santarus, Inc.	RUCONEST is a C1 esterase inhibitor [recombinant] indicated for the treatment of acute attacks in adult and adolescent patients with hereditary angioedema (HAE).	NA	2100 U/1	powder for solution	IV	IV Injection; The recommended dose of RUCONEST is 50 IU per kg with a maximum of 4200 IU to be administered as a slow intravenous injection over approximately 5 minutes.	RUCONEST is contraindicated in patients with a history of allergy to rabbits or rabbit-derived products. RUCONEST is contraindicated in patients with a history of life-threatening immediate hypersensitivity reactions to C1 esterase inhibitor preparations, including anaphylaxis.	The serious adverse reaction in clinical studies of RUCONEST was anaphylaxis. The most common adverse reactions ( Ã¢â€°Â¥ 2%) reported in all clinical trials were headache, nausea, and diarrhea.	Link	NA	NA
10753	Th1175	Desirudin	NA	6963.52	C287H440N80O110 S6	NA	NA	NA	Mean terminal elimination half-life of 2 to 3 hours	Desirudin is a direct, highly selective thrombin inhibitor. Reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation, activation of coagulation factors V, VII, and XIII, and thrombin-induced platelet aggregation resulting in a dose-dependent prolongation of the activated partial thromboplastin time (aPTT).	Preventing blood clots in patients having hip replacement surgery. It may also be used for other conditions as determined by your doctor. Desirudin is a thrombin inhibitor. It works by blocking the activity of thrombin, which helps to prevent the formation of blood clots.	The pharmacodynamic effect of desirudin on proteolytic activity of thrombin was assessed as an increase in aPTT. A mean peak aPTT prolongation of about 1.38 times baseline value (range 0.58 to 3.41) was observed following subcutaneous b.i.d. injections of 15 mg desirudin. Thrombin time (TT) frequently exceeds 200 seconds even at low plasma concentrations of desirudin, which renders this test unsuitable for routine monitoring of Iprivask therapy. At therapeutic serum concentrations, desirudin has no effect on other enzymes of the hemostatic system such as factors IXa, Xa, kallikrein, plasmin, tissue plasminogen activator, or activated protein C. In addition, it does not display any effect on other serine proteases, such as the digestive enzymes trypsin, chymotrypsin, or on complement activation by the classical or alternative pathways.	Desirudin is a direct inhibitor of free circulating and clot-bound thrombin. The anticoagulant properties of desirudin are demonstrated by its ability to prolong the clotting time of human plasma. One molecule of desirudin binds to one molecule of thrombin and thereby blocks the thrombogenic activity of thrombin. As a result, all thrombin-dependent coagulation assays are affected. Activated partial thromboplastin time (aPTT) is a measure of the anticoagulant activity of desirudin and increases in a dose-dependent fashion.	No data available.	Human and animal data suggest that desirudin is primarily eliminated and metabolized by the kidney. The total urinary excretion of unchanged desirudin amounts to 40 to 50% of the administered dose. Metabolites lacking one or two C-terminal amino acids constitute a minor proportion of the material recovered from urine (< 7%). There is no evidence for the presence of other metabolites. This indicates that desirudin is metabolized by stepwise degradation from the C-terminus probably catalyzed by carboxypeptidase(s) such as carboxypeptidase A.	Absorption is complete after subcutaneous administration. Time to peak in plasma is 1 to 3 hours.	0.25 L/kg.	1.5 to 2.7 mL/min/kg.	NA	NA	NA	NA	Abciximab may increase the anticoagulant activities of Desirudin; Acenocoumarol may increase the anticoagulant activities of Desirudin; Acetylsalicylic acid may increase the anticoagulant activities of Desirudin; Alteplase may increase the anticoagulant activities of Desirudin; Anistreplase may increase the anticoagulant activities of Desirudin; Apixaban may increase the anticoagulant activities of Desirudin; Chlorotrianisene may decrease the anticoagulant activities of Desirudin; Citric Acid may increase the anticoagulant activities of Desirudin; The risk or severity of adverse effects can be increased when Desirudin is combined with Collagenase; Dabigatran etexilate may increase the anticoagulant activities of Desirudin.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10754	Th1175	Desirudin	NA	6963.52	C287H440N80O110 S7	NA	NA	NA	Mean terminal elimination half-life of 2 to 3 hours	Desirudin is a direct, highly selective thrombin inhibitor. Reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation, activation of coagulation factors V, VII, and XIII, and thrombin-induced platelet aggregation resulting in a dose-dependent prolongation of the activated partial thromboplastin time (aPTT).	Preventing blood clots in patients having hip replacement surgery. It may also be used for other conditions as determined by your doctor. Desirudin is a thrombin inhibitor. It works by blocking the activity of thrombin, which helps to prevent the formation of blood clots.	The pharmacodynamic effect of desirudin on proteolytic activity of thrombin was assessed as an increase in aPTT. A mean peak aPTT prolongation of about 1.38 times baseline value (range 0.58 to 3.41) was observed following subcutaneous b.i.d. injections of 15 mg desirudin. Thrombin time (TT) frequently exceeds 200 seconds even at low plasma concentrations of desirudin, which renders this test unsuitable for routine monitoring of Iprivask therapy. At therapeutic serum concentrations, desirudin has no effect on other enzymes of the hemostatic system such as factors IXa, Xa, kallikrein, plasmin, tissue plasminogen activator, or activated protein C. In addition, it does not display any effect on other serine proteases, such as the digestive enzymes trypsin, chymotrypsin, or on complement activation by the classical or alternative pathways.	Desirudin is a direct inhibitor of free circulating and clot-bound thrombin. The anticoagulant properties of desirudin are demonstrated by its ability to prolong the clotting time of human plasma. One molecule of desirudin binds to one molecule of thrombin and thereby blocks the thrombogenic activity of thrombin. As a result, all thrombin-dependent coagulation assays are affected. Activated partial thromboplastin time (aPTT) is a measure of the anticoagulant activity of desirudin and increases in a dose-dependent fashion.	No data available.	Human and animal data suggest that desirudin is primarily eliminated and metabolized by the kidney. The total urinary excretion of unchanged desirudin amounts to 40 to 50% of the administered dose. Metabolites lacking one or two C-terminal amino acids constitute a minor proportion of the material recovered from urine (< 7%). There is no evidence for the presence of other metabolites. This indicates that desirudin is metabolized by stepwise degradation from the C-terminus probably catalyzed by carboxypeptidase(s) such as carboxypeptidase A.	Absorption is complete after subcutaneous administration. Time to peak in plasma is 1 to 3 hours.	0.25 L/kg.	1.5 to 2.7 mL/min/kg.	NA	NA	NA	NA	Abciximab may increase the anticoagulant activities of Desirudin; Acenocoumarol may increase the anticoagulant activities of Desirudin; Acetylsalicylic acid may increase the anticoagulant activities of Desirudin; Alteplase may increase the anticoagulant activities of Desirudin; Anistreplase may increase the anticoagulant activities of Desirudin; Apixaban may increase the anticoagulant activities of Desirudin; Chlorotrianisene may decrease the anticoagulant activities of Desirudin; Citric Acid may increase the anticoagulant activities of Desirudin; The risk or severity of adverse effects can be increased when Desirudin is combined with Collagenase; Dabigatran etexilate may increase the anticoagulant activities of Desirudin.	NA	Iprivask	Valeant Pharmaceuticals North America LLC	Valeant Pharmaceuticals North America LLC	Iprivask is indicated for the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism, in patients undergoing elective hip replacement surgery.	NA	NA	NA	Subcutaneous	Initial Dosage: In patients undergoing hip replacement surgery, the recommended dose of Iprivask is 15 mg every 12 hours administered by subcutaneous injection with the initial dose given up to 5 to 15 minutes prior to surgery, but after induction of regional block anesthesia, if used	Iprivask is contraindicated in patients with known hypersensitivity to natural or recombinant hirudins due to risk of anaphylaxis, and in patients with active bleeding and/or irreversible coagulation disorders due to risk of hemorrhage.	Spinal/Epidural Hematoma; Hemorrhagic Events; Increased Risk of Bleeding with Renal Impairment; Antibodies/Re-exposure.	Link	NA	NA
10755	Th1175	Desirudin	NA	6963.52	C287H440N80O110 S8	NA	NA	NA	Mean terminal elimination half-life of 2 to 3 hours	Desirudin is a direct, highly selective thrombin inhibitor. Reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation, activation of coagulation factors V, VII, and XIII, and thrombin-induced platelet aggregation resulting in a dose-dependent prolongation of the activated partial thromboplastin time (aPTT).	Preventing blood clots in patients having hip replacement surgery. It may also be used for other conditions as determined by your doctor. Desirudin is a thrombin inhibitor. It works by blocking the activity of thrombin, which helps to prevent the formation of blood clots.	The pharmacodynamic effect of desirudin on proteolytic activity of thrombin was assessed as an increase in aPTT. A mean peak aPTT prolongation of about 1.38 times baseline value (range 0.58 to 3.41) was observed following subcutaneous b.i.d. injections of 15 mg desirudin. Thrombin time (TT) frequently exceeds 200 seconds even at low plasma concentrations of desirudin, which renders this test unsuitable for routine monitoring of Iprivask therapy. At therapeutic serum concentrations, desirudin has no effect on other enzymes of the hemostatic system such as factors IXa, Xa, kallikrein, plasmin, tissue plasminogen activator, or activated protein C. In addition, it does not display any effect on other serine proteases, such as the digestive enzymes trypsin, chymotrypsin, or on complement activation by the classical or alternative pathways.	Desirudin is a direct inhibitor of free circulating and clot-bound thrombin. The anticoagulant properties of desirudin are demonstrated by its ability to prolong the clotting time of human plasma. One molecule of desirudin binds to one molecule of thrombin and thereby blocks the thrombogenic activity of thrombin. As a result, all thrombin-dependent coagulation assays are affected. Activated partial thromboplastin time (aPTT) is a measure of the anticoagulant activity of desirudin and increases in a dose-dependent fashion.	No data available.	Human and animal data suggest that desirudin is primarily eliminated and metabolized by the kidney. The total urinary excretion of unchanged desirudin amounts to 40 to 50% of the administered dose. Metabolites lacking one or two C-terminal amino acids constitute a minor proportion of the material recovered from urine (< 7%). There is no evidence for the presence of other metabolites. This indicates that desirudin is metabolized by stepwise degradation from the C-terminus probably catalyzed by carboxypeptidase(s) such as carboxypeptidase A.	Absorption is complete after subcutaneous administration. Time to peak in plasma is 1 to 3 hours.	0.25 L/kg.	1.5 to 2.7 mL/min/kg.	NA	NA	NA	NA	Abciximab may increase the anticoagulant activities of Desirudin; Acenocoumarol may increase the anticoagulant activities of Desirudin; Acetylsalicylic acid may increase the anticoagulant activities of Desirudin; Alteplase may increase the anticoagulant activities of Desirudin; Anistreplase may increase the anticoagulant activities of Desirudin; Apixaban may increase the anticoagulant activities of Desirudin; Chlorotrianisene may decrease the anticoagulant activities of Desirudin; Citric Acid may increase the anticoagulant activities of Desirudin; The risk or severity of adverse effects can be increased when Desirudin is combined with Collagenase; Dabigatran etexilate may increase the anticoagulant activities of Desirudin.	NA	Iprivask	Marathon Pharmaceuticals, LLC	Marathon Pharmaceuticals, LLC	Iprivask is indicated for the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism, in patients undergoing elective hip replacement surgery.	NA	NA	NA	NA	Initial Dosage: In patients undergoing hip replacement surgery, the recommended dose of Iprivask is 15 mg every 12 hours administered by subcutaneous injection with the initial dose given up to 5 to 15 minutes prior to surgery, but after induction of regional block anesthesia, if used	Iprivask is contraindicated in patients with known hypersensitivity to natural or recombinant hirudins due to risk of anaphylaxis, and in patients with active bleeding and/or irreversible coagulation disorders due to risk of hemorrhage.	Spinal/Epidural Hematoma; Hemorrhagic Events; Increased Risk of Bleeding with Renal Impairment; Antibodies/Re-exposure.	Link	NA	NA
10773	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Riastap	Csl Behring Gmb H	Csl Behring Gmb H	RiaSTAPÃ¢â€žÂ¢ (fibrinogen concentrate (human) for intravenous use) , Fibrinogen Concentrate (Human) is indicated for the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	NA	Each vial contains 900 to 1300 mg fibrinogen, 400 to 700 mg human albumin, 375 to 660 mg L-arginine hydrochloride, 200 to 350 mg sodium chloride and 50 to 100 mg sodium citrate. Sodium hydroxide and hydrochloric acid may have been used to adjust the pH.	injection, powder, lyophilized, for solution	IV	Dose should be individually calculated for each patient based on the target plasma fibrinogen level based on the type of bleeding, actual measured plasma fibrinogen level and body weight	RiaSTAP (fibrinogen concentrate (human) for intravenous use) is contraindicated in individuals who have manifested severe immediate hypersensitivity reactions, including anaphylaxis to RiaSTAP (fibrinogen concentrate (human) for intravenous use) or its components.	The most serious adverse reactions that have been reported in clinical studies or through postmarketing surveillance following RiaSTAP (fibrinogen concentrate (human) for intravenous use) treatment are allergic-anaphylactic reactions and thromboembolic episodes, including myocardial infarction, pulmonary embolism, deep vein thrombosis, and arterial thrombosis. The most common adverse reactions that have been reported in clinical studies or through postmarketing surveillance following RiaSTAP (fibrinogen concentrate (human) for intravenous use) treatment are allergic reactions and generalized reactions such as chills, fever, nausea, and vomiting.	Link	NA	NA
10774	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Artiss Frozen	Baxter Healthcare Corporation	Baxter Healthcare Corporation	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10775	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Evicel Fibrin Sealant (human)	Ethicon Inc	Ethicon Inc	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10776	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Raplixa	Pro Fibrix Bv	Pro Fibrix Bv	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10777	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Tachosil	Baxter Healthcare Corporation	Baxter Healthcare Corporation	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10778	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Tisseel	Baxter Healthcare Corporation	Baxter Healthcare Corporation	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10779	Th1180	Fibrinogen Concentrate (Human)	NA	340000	NA	NA	NA	NA	78.7 Ã‚Â± 18.13 (55.73-117.26) hours	Fibrinogen Concentrate (Human) is a heat-treated, lyophilized fibrinogen (coagulation factor I) powder made from pooled human plasma.	For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia.	Administration of fibrinogen concentrate (human) for intravenous use to patients with congenital fibrinogen deficiency replaces the missing, or low coagulation factor. Normal levels are in the range of 200 to 450 mg/dL	Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (AÃŽÂ±, BÃŽÂ² and ÃŽÂ³). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the AÃŽÂ± and BÃŽÂ² chains releasing fibrinopeptides A and B (FPA and FPB, respectively).2 FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers.2 The resulting fbrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis.3 Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.	NA	NA	NA	NA	NA	NA	NA	NA	NA	The risk or severity of adverse effects can be increased when Aminocaproic Acid is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Menadione is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Phylloquinone is combined with Fibrinogen Concentrate (Human); The risk or severity of adverse effects can be increased when Tranexamic Acid is combined with Fibrinogen Concentrate (Human).	NA	Tisseel Frozen	Baxter Healthcare Corporation	Baxter Healthcare Corporation	NA	NA	NA	NA	NA	NA	NA	NA	Link	NA	NA
10783	Th1182	Gastric intrinsic factor	NA	NA	NA	NA	NA	NA	NA	Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 (cobalamin) later on in the small intestine.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA
10784	Th1182	Gastric intrinsic factor	NA	NA	NA	NA	NA	NA	NA	Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 (cobalamin) later on in the small intestine.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	Hematogen	Nnodum Pharmaceuticals	Nnodum Pharmaceuticals	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA
10785	Th1183	Hepatitis B immune globulin	NA	NA	NA	NA	NA	NA	22-25 days	Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus.	Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications.	NA	In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	HBsAg	NA	NA	NA	NA	NA	220 [iU]/mL, 1560 [iU]/5mL, 312 [iU]/mL - Injections; 312 [iU]/mL, 50 mg/mL - Injections solutions	Injection; Solution	Intra muscular; IV	NA	NA	NA	NA	NA	NA
10786	Th1183	Hepatitis B immune globulin	NA	NA	NA	NA	NA	NA	22-25 days	Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus.	Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications.	NA	In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	HBsAg	Hepagam B	Cangene Bio Pharma Inc.	Cangene Bio Pharma Inc.	HepaGam BÃ¢â€žÂ¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients.	NA	50 mg/mL	injection, solution	intramuscular; intravenous	Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam BÃ¢â€žÂ¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended	Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks.	The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain.	Link	NA	NA
10787	Th1183	Hepatitis B immune globulin	NA	NA	NA	NA	NA	NA	22-25 days	Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus.	Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications.	NA	In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	HBsAg	Hepagam B	Cangene Bio Pharma Inc.	Cangene Bio Pharma Inc.	HepaGam BÃ¢â€žÂ¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients.	NA	50 mg/mL	injection, solution	intramuscular; intravenous	Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam BÃ¢â€žÂ¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended	Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks.	The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain.	Link	NA	NA
10788	Th1183	Hepatitis B immune globulin	NA	NA	NA	NA	NA	NA	22-25 days	Long-term hepatitis B immune globulin (HBIG) has been shown to reduce hepatitis B virus (HBV) reinfection in patients transplanted for hepatitis B. Infection with hepatitis B may lead to hepatocellular carcinoma, a type of liver cancer. Therefore, the hepatitis-B vaccines are cancer-preventing vaccines. According to the Centers for Disease Control and Prevention (CDC), the hepatitis B vaccine was the first anti-cancer vaccine. HBIG is prepared from the plasma of donors who have high antibody levels of the hepatitis B surface antigen. It is extracted from the Cohn fraction II. During the process, viruses are deactivated, and in the final steps, solvents used in the preparation are removed. The preparation is tested for absence of HIV, HCV, herpes virus, and reovirus.	Investigated for use/treatment in hepatitis (viral, B), liver transplant surgery, and pediatric indications.	NA	In countries with high rates of hepatitis B infection, vaccination of newborns has not only reduced the risk of infection, but has also led to marked reduction in liver cancer.	NA	NA	NA	NA	NA	NA	NA	NA	NA	NA	HBsAg	Hepagam B	Cangene Bio Pharma Inc.	Cangene Bio Pharma Inc.	HepaGam BÃ¢â€žÂ¢, Hepatitis B Immune Globulin Intravenous (Human), is indicated for the prevention of hepatitis B recurrence following liver transplantation, in HBsAg-positive liver transplant patients.	NA	312 [iU]/mL	injection, solution	intramuscular; intravenous	Based upon the HepaGam B (hepatitis b immune globulin (human)) clinical trial, patients should receive 20,000 lU/dose [see Clinical Trials in Liver Transplant Patients]. The volume of each 20,000 IU dose should be calculated from the measured potency of the particular lot of HepaGam BÃ¢â€žÂ¢ (Hepatitis B Immune Globulin Intravenous [Human]) as stamped on the vial label. The first dose should be administered concurrently with the grafting of the transplanted liver (the anhepatic phase) with subsequent dosing as recommended	Individuals known to have anaphylactic or severe systematic reactions associated with the parenteral administration of human globulin preparations should not receive HepaGam B (hepatitis b immune globulin (human)) , (Hepatitis B Immune Globulin Intravenous [Human]), or any other human immune globulin. HepaGam B (hepatitis b immune globulin (human)) contains less than 40 micro-grams/mL of IgA. Individuals who are deficient in IgA may have the potential to develop IgA antibodies and have an anaphylactoid reaction. The physician must weigh the potential benefit of treatment with HepaGam B (hepatitis b immune globulin (human)) against the potential for hypersensitivity reactions. For postexposure prophylaxis indications, HepaGam B (hepatitis b immune globulin (human)) must be administered intramuscularly only. In patients who have severe thrombocytopenia or any coagulation disorder that would contraindicate intramuscular injections, HepaGam B (hepatitis b immune globulin (human)) should be given only if the expected benefits outweigh the potential risks.	The most common expected adverse drug reactions for intravenous immune globulins like HepaGam B (hepatitis b immune globulin (human)) are chills, fever, headaches, vomiting, allergic reactions, nausea, arthralgia and moderate low back pain.	Link	NA	NA

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