Browse result page of ThPDB2
This is the result page of the browse module of ThPDB2. This page gives the information about the query submitted by the user as per the browse category. Further details of the entries can be seen by clicking on the ID or THPP_ID. Further the user can sort the entries on the basis of various fields by clicking on the respective headers. The user can also download the results in various formats.
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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 |
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| 10499 | Th1095 | Ranibizumab | >Th1095_Ranibizumab EVQLVESGGGLVQPGGSLRLSCAASGYDFTHYGMNWVRQAPGKGLEWVGWINTYTGEPTYAADFKRRFTFSLDTSKSTAYLQMNSLRAEDTAVYYCAKYPYYYGTSHWYFDVWGQGTLVTVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHL | 48349.61 | C2158H3282N562O681S12 | NA | NA | NA | Approximately 9 days. | Recombinant (E.coli derived), humanized IgG1 kappa isotype monoclonal antibody (intraocular use). It binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab is marketed under the name Lucentis. | For the treatment of patients with macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. | Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab is a VEGF-A antagonist that binds to and inhibits the biologic activity of active forms of human VEGF-A, including the cleaved form (VEGF110). VEGF-A has been shown to cause neovascularization (angiogenesis) and an increase in vascular permeability, which is thought to contribute to the progression of the neovascular form of age-related macular degeneration (AMD). | Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, (VEGF110). The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation. | There is no information available regarding the LD50 values of ranibizumab. There is also limited clinical experience of ranibizumab overdose: concentrated doses as high as 2 mg ranibizumab in 0.05 mL have been administered to patients, with no additional unexpected adverse reactions that were observed | The metabolism of ranibizumab has not been studied. Since it is a monoclonal antibody fragment, ranibizumab is expected to undergo catabolism. | Ranibizumab rapidly penetrates through the retina to reach the choroid after intravitreal injection. Following monthly intravitreal administration of 0.5 mg ranibizumab in patients with neovascular (wet) age-related macular degeneration, the mean Cmax (±SD) was 1.7 (± 1.1) ng/mL. Following an implant insertion, the mean (±SD) Cmax of ranibizumab was 0.48 (±0.17) ng/mL and median Tmax was 26 days, with a range of one to 89 days. | The apparent volume of the central compartment (Vd/F) is 2.77 L. Ranibizumab is not shown to accumulate in serum. Due to its small size from lacking the Fc region of an antibody, ranibizumab achieves enhanced diffusion into the retina and choroid | In patients with retinal vein occlusion or diabetic macular edema, the apparent clearance (CL/F) of ranibizumab was 24.8 L/day. | Amino Acids, Peptides, and Proteins,Angiogenesis Inhibitors,Angiogenesis Modulating Agents,Antibodies,Antibodies, Monoclonal,Antibodies, Monoclonal, Humanized,Antineovascularisation Agents,Blood Proteins,EENT Drugs, Miscellaneous,Globulins,Growth Inhibitors,Growth Substances,Immunoglobulins,Immunoproteins,Ocular Vascular Disorder Agents,Ophthalmics,Ophthalmologicals,Proteins,Sensory Organs,Serum Globulins,Vascular Endothelial Growth Factor Inhibitor,Vascular Endothelial Growth Factor Inhibitors | CA2286330 | 10-Jun-2008 | 3-Apr-2018 | NA | Vascular endothelial growth factor A | Lucentis | Genentech | Genentech | Neovascular (Wet) Age-Related Macular Degeneration (AMD), Macular Edema Following Retinal Vein Occlusion (RVO), Diabetic Macular Edema (DME), Diabetic Retinopathy (Non Proliferative Diabetic Retinopathy (NPDR), Proliferative Diabetic Retinopathy (PDR)) In patients With Diabetic Macular Edema (DME) | NA | supplied as a preservative-free, sterile solution in a single-use glass vial designed to deliver 0.05 mL of 10 mg/mL LUCENTIS (0.5 mg dose vial) or 6 mg/mL LUCENTIS (0.3 mg dose vial) aqueous solution with 10 mM histidine HCl, 10% α,α-trehalose dihydrate, 0.01% polysorbate 20, pH 5.5. | Sterile, colorless to pale yellow solution in a single-use glass vial | Intravitreal Injection ONLY | Neovascular (Wet) Age-Related Macular Degeneration (AMD): LUCENTIS 0.5 mg (0.05 mL of 10 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). LUCENTIS 0.5 mg (0.05 mL of 10 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). Diabetic Macular Edema (DME): LUCENTIS 0.3 mg (0.05 mL of 6 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days).; Diabetic Retinopathy In Patients With Diabetic Macular Edema: LUCENTIS 0.3 mg (0.05 mL of 6 mg/mL LUCENTIS solution) is recommended to be administered by intravitreal injection once a month (approximately 28 days). | Ocular Or Periocular Infections LUCENTIS is contraindicated in patients with ocular or periocular infections. Hypersensitivity to ranibizumab or any of the excipients in LUCENTIS. Hypersensitivity reactions may manifest as severe intraocular inflammation. | Endophthalmitis and Retinal Detachments Increases in Intraocular Pressure, Thromboembolic Events, Fatal Events in patients with DME and DR at baseline. | Link | NA | NA |
| 10556 | Th1108 | Pegaptanib | NA | 541.6 | C22H44N3O10P | NA | NA | NA | 10 ± 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 μL. 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 |
| 10643 | Th1133 | Aflibercept | >Th1133_Aflibercept SDTGRPFVEMYSEIPEIIHMTEGRELVIPCRVTSPNITVTLKKFPLDTLIPDGKRIIWDSRKGFIISNATYKEIGLLTCEATVNGHLYKTNYLTHRQTNTIIDVVLSPSHGIELSVGEKLVLNCTARTELNVGIDFNWEYPSSKHQHKKLVNRDLKTQSGSEMKKFLSTLTIDGVTRSDQGLYTCAASSGLMTKKNSTFVRVHEKDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPG | 115000 | C4318H6788N1164O1304S32 | NA | NA | NA | Intravitreal half life - 7.13 days | Aflibercept is a vascular endothelial growth factor (VEGF) inhibitor. It is a recombinant dimeric fusion glycoprotein that comprises (VEGF) binding portions from the extracellular domains of human VEGF receptors 1 and 2, this is fused to the Fc portion of human IgG1. It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa (protein part = 96.9 kDa). It has 5 putative N-glycosylation sites on each polypeptide chain and the attached carbohydrates exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the site associated with the Fc domain, which is unsialylated. | The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin. | Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM). | Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. | For all intravitreal VEGF inhibitors, there is increased risk of stroke and myocardial infarction. An increase in intraocular pressure may also occur. When used intravenously, most common adverse reactions were leukopenia, diarrhea, neutropenia, proteinuria, AST increased, stomatitis, fatigue, thrombocytopenia, ALT increased, hypertension, weight decreased, decreased appetite, epistaxis, abdominal pain, dysphonia, serum creatinine increased, and headache. | Because aflibercept is a protein, it is expected to be broken down via proteolysis into smaller peptides and amino acids. The cytochrome P450 enzyme system is not involved in the metabolism of aflibercept. | In patients with wet AMD and CRVO, the mean peak plasma concentration (Cmax) was 0.02 mcg/mL and 0.05 mcg/mL respectively. These concentrations were reached in 1 to 3 days. Aflibercept did not accumulate when administered as repeated doses intravitreally every 4 weeks. | After intravenous injection of aflibercept, the volume of distribution is 6 L. | When cancer patients were given 2-9 mg/kg every 2 or 3 week; 1 hour IV infusion of aflibercept the typical estimated clearances were as follows: CL of free aflibercept (CLf) = 0.88 L/day; CL of bound aflibercept (CLf) = 0.19 L/day; Patients clear free aflibercept faster if they had low albumin or high alkaline phosphatase levels. | Antineoplastic Agents and Ophthalmics | US7306799 | 12-Nov-2007 | 23-05-2020 | NA | Vascular endothelial growth factor A,Placenta growth factor,Vascular endothelial growth factor B | Eylea | Regeneron Pharmaceuticals | Regeneron Pharmaceuticals | Neovascular (Wet) Age-Related Macular Degeneration (AMD), Macular Edema Following Central Retinal Vein Occlusion (CRVO) | NA | EYLEA is supplied as a preservative-free, sterile, aqueous solution in a single-use, glass vial designed to deliver 0.05 mL (50 microliters) of EYLEA (40 mg/mL in 10 mM sodium phosphate, 40 mM sodium chloride, 0.03% polysorbate 20, and 5% sucrose, pH 6.2). | EYLEA is a sterile, clear, and colorless to pale yellow solution. | Intravitreal Injection | The recommended dose for EYLEA is 2 mg (0.05 mL or 50 microliters) administered by intravitreal injection every 4 weeks (monthly) for the first 12 weeks (3 months), followed by 2 mg (0.05 mL) via intravitreal injection once every 8 weeks (2 months). | ocular or periocular infections, active intraocular inflammation, Hypersensitivity | Endophthalmitis and retinal detachments, Increased intraocular pressure, Thromboembolic events | Link | NA | NA |
| 10650 | Th1135 | Ocriplasmin | >Th1135_Ocriplasmin APSFDCGKPQVEPKKCPGR | 27250 | C1214H1890N338O348S14 | NA | NA | NA | NA | Ocriplasmin is a recombinant (derived from Pichia pastoris) truncated form of human plasmin with a molecular weight of 27.2 kDa. It is a 249 amino acid protein that is made up of two peptide chains. Agent for pharmacologic vitreolysis; thrombolytic agent. FDA approved on October 17, 2012. | Ocriplasmin is a proteolytic enzyme indicated for the treatment for symptomatic vitreomacular adhesion. | NA | Ocriplasmin has proteolytic activity against protein components of the vitreous body and the vitreoretinal interface (VRI) (e.g. laminin, fibronectin and collagen), thereby dissolving the protein matrix responsible for the vitreomacular adhesion (VMA). | The most commonly reported reactions (= 5%) in patients treated with ocriplasmin were vitreous floaters, conjunctival hemorrhage, eye pain, photopsia, blurred vision, macular hole, reduced visual acuity, visual impairment, and retinal edema. | Ocriplasmin is quickly inactivated by protease inhibitor a2-antiplasmin or a2-macroglobulin. | Because of the small dose administered (0.125 mg), ocriplasmin is not expected to be in the systemic circulation following injection. Within 30 minutes after injection, levels of ocriplasmin in the vitreous are 12 mcg/mL. 24 hours after injection, levels in the virtreous are 0.5 mcg/mL | NA | NA | Ophthalmics | NA | NA | NA | NA | Fibronectin,Alpha-2-macroglobulin,Alpha-2-antiplasmin | Jetrea | ThromboGenics NV | ThromboGenics NV | symptomatic vitreomacular adhesion. | NA | Each vial contains 0.5 mg ocriplasmin (active) and 0.21 mg citric acid, 0.75 mg mannitol, sodium hydroxide (for pH adjustment) and water for injection. The pH of the solution is 3.1. | JETREA is a Sterile, clear and colorless solution with no preservatives | Intravitreal Injection | 0.125 mg (0.1 mL of the diluted solution) | NA | Decreased Vision, Intravitreal Injection Procedure Associated Effects, Potential for Lens Subluxation, Retinal Breaks | Link | NA | NA |