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.
Tabular representation:
| 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 |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 10187 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | Neosporin | Pfizer | Pfizer | Neosporin ointment is an antibiotic combination which works by killing sensitive bacteria on the skin or in wounds.Thus, treating and preventing infection due to minor cuts, scrapes, and burns. | NA | Each gram contains: neomycin sulfate equivalent to 3.5 mg neomycin base, polymyxin B sulfate equivalent to 10,000 polymyxin B units, bacitracin zinc equivalent to 400 bacitracin units, and white petrolatum, q.s. | Ointment | External use only | Apply the ointment every 3 or 4 hours for 7 to 10 days depending on the severity of the infection. | Individuals who have shown hypersensitivity to any of its components | Rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue; skin irritation, pain, burning, cracking, redness, or peeling not present before using Neosporin ointment; worsening or recurrence of wound symptoms. | Link | NA | NA |
| 10188 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10189 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10190 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | Sofradex | Sanofi | Sanofi | Used in the eye(s) to treat Inflammation in the eye when prevention of bacterial infection is also needed. Signs include sore, red or swollen eyes. It is used in the ear(s) to treat Inflammation of the ear canal (otitis externa) | NA | Each bottle contains 0.5% w/v of Framycetin Sulphate, Dexamethasone Sodium Metasulphobenzoate (equivalent to 0.050% w/v of Dexamethasone) and 0.005% w/v of Gramicidin. The other ingredients are citric acid, sodium citrate, lithium chloride, phenylethyl al | Sterile, clear, bright, colourless, aqueous solution | Auricular and Ocular use. | One or two drops applied to each affected eye up to six times daily or more frequently if required. Two or three drops instilled into the ear three or four times daily. | If glaucoma is present or herpetic keratitis (e.g. dendritic ulcer) is considered a possibility. Otitis Externa should not be treated when the eardrum is perforated because of the risk of ototoxicity. Hypersensitivity to framycetin sulphate, dexamethasone sodium metasulphobenzoate, gramicidin or to any of the excipients. | Stop using Sofradex if: You get any kind of skin problem, such as a rash or itching around your eyes or irritation burning, stinging, itching or swelling, your eyes have problems focussing or develop a blind spot. You may have increased pressure in the eye, you have difficulty seeing at night or notice that your eyesight is cloudy and fuzzy, or you see halos around lights. These could be signs of cataracts. This may occur after using the medicine for a long time | Link | NA | NA |
| 10191 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10192 | Th1024 | Gramicidin D | >Th1024_Gramicidin_D VGALAVVVWLWLWLWX | 1811.253 | C96H135N19O16 | NA | NA | 229 | NA | Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids. The peptides assemble inside of the hydrophobic interior of the cellular lipid bilayer to form an alpha helix. The helix itself is not long enough to span the membrane but it dimerizes to form the elongated channel needed to span the whole membrane. Gramicidin D is used primarily as a topical antibiotic and is one of the three constituents of consumer antibiotic polysporin ophthalmic solution. | For treatment of skin lesions, surface wounds and eye infections | Gramicidin is particularly effective against gram-positive bacteria because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution | Gramicidin D binds and inserts itself into bacterial membranes (preference to gram-positive cell membranes) resulting in membrane disruption and permeabilization (it acts as a channel). This leads to loss of intracellular solutes (e.g., K+ and amino acids); dissipation of the transmembrane potential; inhibition of respiration; a reduction in ATP pools; and inhibition of DNA, RNA, and protein synthesis, which leads to cell death. | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins, Anti-Bacterial Agents, Anti-Infective Agents, Anti-Infective Agents, Local, Membrane Proteins, P-glycoprotein inhibitors, P-glycoprotein substrates, Peptides, Peptides, Cyclic, Pore Forming Cytotoxic Proteins, Proteins, Throat Preparations | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 10419 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.5 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | CA2280565 | 15-Nov-2005 | 20-Aug-2019 | NA | Synaptosomal-associated protein 25,Rho-related GTP-binding protein RhoB | BOTOX | Allergan | Allergan | Prescribed in cases such as Bladder Dysfunction, Chronic Migraine, Upper Limb Spasticity, Cervical Dystonia, Primary Axillary Hyperhidrosis, Blepharospasm and Strabismus | NA | Each vial of BOTOX contains either 50 Units of Clostridium botulinum type A neurotoxin complex, 0.25 mg of Albumin Human, and 0.45 mg of sodium chloride; 100 Units of Clostridium botulinum type A neurotoxin complex, 0.5 mg of Albumin Human, and 0.9 mg of sodium chloride; or 200 Units of Clostridium botulinum type A neurotoxin complex, 1 mg of Albumin Human, and 1.8 mg of sodium chloride in a sterile, vacuum-dried form without a preservative. | BOTOX (onabotulinum toxin A) For Injection is a sterile, vacuum-dried purified botulinum toxin type A, produced from fermentation of Hall strainClostridium botulinum type A | IntramuSubcutaneousular, intradetrusor and intrade | Do not exceed a total dose of 360 Units administered in a 3 month interval. | Known Hypersensitivity to Botulinum Toxin, Infection at the Injection Site, Urinary Tract Infection or Urinary Retention. | Spread of Toxin Effects, Hypersensitivity, Dysphagia and Breathing Difficulties in Treatment of Cervical Dystonia, Bronchitis and Upper Respiratory Tract Infections in Patients Treated for Spasticity, Urinary Retention in Patients Treated for Bladder Dysfunction. | Link | NA | NA |
| 10420 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.6 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | CA2310845 | 15-May-2001 | 7-Jun-2014 | NA | Growth hormone receptor | Dysport | Ipsen Pharmaceuticals | Ipsen Pharmaceuticals | Dysport is indicated for the treatment of Cervical Dystonia and Glabellar Lines | NA | Each vial contains 500 or 300 Units of lyophilized abobotulinumtoxinA, 125 micrograms human serum albumin and 2.5 mg lactose. Dysport may contain trace amounts of cow's milk proteins | Dysport is supplied in a single-use, sterile vial for reconstitution | IntramuSubcutaneousular Injection | In Cervical Dystonia: Initial dose of DYSPORT  is 500 Units given intramuscularly. Re-treatment every 12 to 16 weeks or longer, as necessary, based on return of clinical symptoms with doses administered between 250 and 1000 Units to optimize clinical benefit. In Glabellar Lines: A total dose of 50 Units of DYSPORT , divided in five equal aliquots of 10 Units each, should be administered to affected muscles to achieve clinical effect. | DYSPORT is contraindicated in patients with known hypersensitivity to any botulinum toxin preparation or to any of the components in the formulation. | In Cervical Dystonia: Most commonly observed adverse reactions (> 5% of patients) are: muscular weakness, dysphagia, dry mouth, injection site discomfort, fatigue, headache, neck pain, musculoskeletal pain, dysphonia, injection site pain, and eye disorders. In Glabellar Lines: The most frequently reported adverse events (≥2%) are nasopharyngitis, headache, injection site pain, injection site reaction, upper respiratory tract infection, eyelid edema, eyelid ptosis, sinusitis and nausea. | Link | NA | NA |
| 10421 | Th1070 | Botulinum Toxin Type A | >Th1070_Botulinum_Toxin_Type_A MPFVNKQFNYKDPVNGVDIAYIKIPNVGQMQPVKAFKIHNKIWVIPERDTFTNPEEGDLNPPPEAKQVPVSYYDSTYLSTDNEKDNYLKGVTKLFERIYSTDLGRMLLTSIVRGIPFWGGSTIDTELKVIDTNCINVIQPDGSYRSEELNLVIIGPSADIIQFECKSFGHEVLNLTRNGYGSTQYIRFSPDFTFGFEESLEVDTNPLLGAGKFATDPAVTLAHELIHAGHRLYGIAINPNRVFKVNTNAYYEMSGLEVSFEELRTFGGHDAKFIDSLQENEFRLYYYNKFKDIASTLNKAKSIVGTTASLQYMKNVFKEKYLLSEDTSGKFSVDKLKFDKLYKMLTEIYTEDNFVKFFKVLNRKTYLNFDKAVFKINIVPKVNYTIYDGFNLRNTNLAANFNGQNTEINNMNFTKLKNFTGLFEFYKLLCVRGIITSKTKSLDKGYNKALNDLCIKVNNWDLFFSPSEDNFTNDLNKGEEITSDTNIEAAEENISLDLIQQYYLTFNFDNEPENISIENLSSDIIGQLELMPNIERFPNGKKYELDKYTMFHYLRAQEFEHGKSRIALTNSVNEALLNPSRVYTFFSSDYVKKVNKATEAAMFLGWVEQLVYDFTDETSEVSTTDKIADITIIIPYIGPALNIGNMLYKDDFVGALIFSGAVILLEFIPEIAIPVLGTFALVSYIANKVLTVQTIDNALSKRNEKWDEVYKYIVTNWLAKVNTQIDLIRKKMKEALENQAEATKAIINYQYNQYTEEEKNNINFNIDDLSSKLNESINKAMININKFLNQCSVSYLMNSMIPYGVKRLEDFDASLKDALLKYIYDNRGTLIGQVDRLKDKVNNTLSTDIPFQLSKYVDNQRLLSTFTEYIKNIINTSILNLRYESNHLIDLSRYASKINIGSKVNFDPIDKNQIQLFNLESSKIEVILKNAIVYNSMYENFSTSFWIRIPKYFNSISLNNEYTIINCMENNSGWKVSLNYGEIIWTLQDTQEIKQRVVFKYSQMINISDYINRWIFVTITNNRLNNSKIYINGRLIDQKPISNLGNIHASNNIMFKLDGCRDTHRYIWIKYFNLFDKELNEKEIKDLYDNQSNSGILKDFWGDYLQYDKPYYMLNLYDPNKYVDVNNVGIRGYMYLKGPRGSVMTTNIYLNSSLYRGTKFIIKKYASGNKDNIVRNNDRVYINVVVKNKEYRLATNASQAGVEKILSALEIPDVGNLSQVVVMKSKNDQGITNKCKMNLQDNNGNDIGFIGFHQFNNIAKLVASNWYNRQIERSSRTLGCSWEFIPVDDGWGERPL | 900000 | C6760H10447N1743O2010S32 | 5.6 | -0.368 | 85.5-86.7 | 230 to 260 min in a pharmacokinetic study of rats and mice | Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. | For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. | A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. | Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. | Based on toxicological studies, it has been estimated that the human LD50 by injection is approximately 2800 Units, equivalent to 28 individual vials of BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex (100 Units) for a 70 kg adult. When injected intramuscularly, Botulinum Toxin Type A has been shown to be teratogenic or to have embryocidal effects in some animal species. | NA | The chemical complexity of Botulinum Toxin Type A combined with its extreme potency limits the opportunity to study its pharmacokinetic profile in humans. Therefore, no human pharmacokinetic studies have been performed. Botulinum Toxin Type A is injected directly into the target organ, a skeletal muscle. Thus, bioavailability of the intravenous or oral route is not of clinical relevance. | NA | NA | Acetylcholine Release Inhibitors, Agents that produce neuromuscular block (indirect), Amino Acids, Peptides, and Proteins, Bacterial Proteins, Bacterial Toxins, Biological Factors, Botulinum Toxins, Botulinum Toxins, Type A, Central Nervous System Depressants, Cholinergic Agents, Endopeptidases, Enzymes, Enzymes and Coenzymes, Ganglion Blockers, Hydrolases, Membrane Transport Modulators, Metalloendopeptidases, Metalloproteases, Muscle Relaxants, Muscle Relaxants, Peripherally Acting Agents, Musculo-Skeletal System, Neuromuscular Agents, Neuromuscular Blocking Agents, Neurotoxins, Neurotransmitter Agents, Noxae, Other Miscellaneous Therapeutic Agents, Peptide Hydrolases, Peripheral Nervous System Agents, Proteins, Toxic Actions, Toxins, Biological | NA | NA | NA | NA | NA | Xeomin | MERZ AESTHETICS | MERZ AESTHETICS | Xeomin is indicated in Cervical Dystonia, Blepharospasm, Glabellar Lines | NA | One vial of XEOMIN contains 50 or 100 Units of incobotulinumtoxinA, 1 mg of human albumin, and 4.7 mg sucrose. | XEOMIN is a sterile white to off-white lyophilized powder after reconstitution with preservative-free 0.9% Saline for Injection. | IntramuSubcutaneousular Injection | In Cervical Dystonia: Initial dose of Xeomin is 120 Units given intramuscularly. In Blepharospasm: The total initial dose of XEOMIN in both eyes should not exceed 70 Units (35 Units/eye).In Glabellar Lines: The total recommended XEOMIN dose is 20 Units per treatment session divided into five equal intramuscular injections of 4 Units each. | Known hypersensitivity to the active substance botulinum neurotoxin type A or to any of the excipients and Infection at the proposed injection sites | In Cervical Dystonia: The most commonly observed adverse reactions (≥5% of patients and > placebo) are dysphagia, neck pain, muscle weakness, injection site pain, and musculoskeletal pain. In Blepharospasm: The most commonly observed adverse reactions (≥5% of patients and > placebo) are eyelid ptosis, dry eye, dry mouth, diarrhea, headache, visual impairment, dyspnea, nasopharyngitis, and respiratory tract infection. In Glabellar Lines:The most commonly observed adverse reaction (>1% of patients and > placebo) is headache. | Link | NA | NA |
| 12181 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12182 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Biological Factors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12183 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Intercellular Signaling Peptides and Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12184 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Nerve Growth Factors | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12185 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Nerve Tissue Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12186 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Peptides | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12187 | Th1296 | Ciliary neurotrophic factor | >Th1296_Ciliary_neurotrophic_factor MAFTEHSPLTPHRRDLCSRSIWLARKIRSDLTALTESYVKHQGLNKNINLDSADGMPVASTDQWSELTEAERLQENLQAYRTFHVLLARLLEDQQVHFTPTEGDFHQAIHTLLLQVAAFAYQIEELMILLEYKIPRNEADGMPINVGDGGLFEKKLWGLKVLQELSQWTVRSIHDLRFISSHQTGIPARGSHYIANNKKM | NA | NA | NA | NA | NA | NA | Ciliary neurotrophic factor (NT-501) is Neurotech's lead product which is in two Phase II/III clinical trials for the treatment of visual loss associated with retinitis pigmentosa and a Phase II trial for the treatment of the dry form of age-related macular degeneration. Neurotech is also evaluating other factors that can be used with its proprietary delivery technology, Encapsulated Cell Technology (ECT), to treat additional retinal diseases. | Investigated for use/treatment in eye disorders/infections, macular degeneration, and retinal disorders (unspecified). | NA | NT-501 is an intraocular, cell containing polymer implant designed to provide the continuous, long-term release of the therapeutic protein, Ciliary Neurotrophic Factor (CNTF), directly into the back of the eye by means of the Company's proprietary Encapsulated Cell Technology (ECT). | NA | NA | NA | NA | NA | Proteins | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12747 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Amino Acids, Peptides, and Proteins | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | Tepezza | Horizon Therapeutics USA, Inc. | Horizon Therapeutics USA, Inc. | Intravenous | 500 mg/1 | None | muscle spasm, nausea, hair loss, diarrhea, fatigue, high blood sugar (hyperglycemia), hearing impairment, dry skin, changes in taste, and headache | Tepezza is an insulin-like growth factor-1 receptor inhibitor (IGF-1R). Tepezza is used to treat thyroid eye disease (sometimes called Graves Eye Disease). Thyroid eye disease is an autoimmune disorder in which the immune system attacks tissues around the eyes. Symptoms include dry or watery eyes, eye... | Tepezza (teprotumumab-trbw) is an insulin-like growth factor-1 receptor inhibitor used to treat Thyroid Eye disease. | NA | NA | Link | Link | NA |
| 12748 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Antibodies | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12749 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Globulins | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12750 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Hyperglycemia-Associated Agents | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12751 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Immunoproteins | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12752 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Insulin-like Growth Factor-1 Receptor Inhibitor | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12753 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Insulin-like Growth Factor-1 Receptor Inhibitors | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12754 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Ototoxic agents | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |
| 12755 | Th1351 | Teprotumumab | >Th1351_Teprotumumab QVELVESGGGVVQPGRSQRLSCAASGFTFSSYGMHWVRQAPGKGLEWVAIIWFDGSSTYYADSVRGRFTISRDNSKNTLYLQMNSLRAEDTAVYFCARELGRRYFDLWGRGTLVSVSSASTKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSGLYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGK | 148000 | NA | NA | NA | NA | The half-life of teprotumumab is 20 ± 5 days.[L11359] | Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor.[L11359] Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received "breakthrough therapy" designation from the FDA in 2016[A190129] and was approved by the FDA in January 2020 for the treatment of TED.[L11350] Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease.[L11350] | Teprotumumab is indicated for the treatment of thyroid eye disease.[L11359] | Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease.[L11359,A190138] Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab.[L11359] | Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin.[A190138] One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy.[A189937] It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients.[A190138] It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.[A190138] Teprotumumab is a fully human IgG1 monoclonal antibody directed against IGF-1R. It binds to and induces internalization and degradation of these receptors,[A189937] thus preventing their downstream effects and alleviating symptoms of thyroid eye disease.[L11359] | Toxicity information, including information regarding overdosage, is currently unavailable.[L11359] Symptoms of teprotumumab overdose are likely to be consistent with its adverse effect profile. | The metabolism of teprotumumab has not been fully characterized. As a protein, its metabolism is expected to involve proteolysis to smaller proteins and peptides.[L11359] | In a population of 40 patients receiving standard dosing in two clinical trials of teprotumumab, utilizing a two-compartment pharmacokinetic model, the AUC and Cmax were estimated to be 138 ± 34 mg•hr/mL and 632 ± 139 mcg/mL, respectively.[L11359] | Following the standard dosing regimen, the mean central and peripheral volumes of distribution are approximately 3.26 ± 0.87 L and 4.32 ± 0.67 L, respectively.[L11359] | The estimated mean clearance of teprotumumab is 0.27 L/day.[L11359] The inter-compartment clearance is 0.74 L/day.[L11359] | Proteins | NA | NA | NA | NA | Insulin-like growth factor 1 receptor | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | NA | Link | NA | NA |