Identification

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Name
Lorlatinib
Accession Number
DB12130
Type
Small Molecule
Groups
Approved, Investigational
Description

Lorlatinib has been used in trials studying the basic science and treatment of Non-small Cell Lung Cancer and anaplastic lymphoma kinase (ALK)-positive Non-Small Cell Lung Cancer (NSCLC) and ROS1-positive NSCLC. Despite initial responses from the use of various ALK inhibitors, however, it is virtually almost guaranteed that all patients with the condition in question will develop tumour progression or resistance to the current therapy in use 9.

Considered a third-generation ALK tyrosine kinase inhibitor (TKI) for patients with ALK-positive metastatic NSCLC, lorlatinib's most optimal place in the treatment sequence of this condition has most recently been identified with its latest approval by the US FDA in November of 2018 for the indication of treating those patients' disease which has progressed even after the use of first and second-generation TKIs like crizotinib, alectinib, or ceritinib 10,Label. Loratinib's ability to move past the blood-brain barrier facilitates its ability to treat progressive or worsening brain metastases as well 10,5.

Structure
Thumb
Synonyms
  • Lorlatinib
External IDs
PF 06463922 / PF-06463922
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
LorbrenaTablet100 mgOralPfizer Canada UlcNot applicableNot applicableCanada
LorbrenaTablet25 mgOralPfizer Canada UlcNot applicableNot applicableCanada
LorbrenaTablet, film coated100 mg/1OralPfizer Laboratories Div Pfizer Inc2018-11-19Not applicableUs
LorbrenaTablet, film coated25 mg/1OralPfizer Laboratories Div Pfizer Inc2018-11-19Not applicableUs
Additional Data Available
  • Application Number
    Application Number

    A unique ID assigned by the FDA when a product is submitted for approval by the labeller.

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  • Product Code
    Product Code

    A governmentally-recognized ID which uniquely identifies the product within its regulatory market.

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Categories
UNII
OSP71S83EU
CAS number
1454846-35-5
Weight
Average: 406.421
Monoisotopic: 406.155352039
Chemical Formula
C21H19FN6O2
InChI Key
IIXWYSCJSQVBQM-LLVKDONJSA-N
InChI
InChI=1S/C21H19FN6O2/c1-11-15-7-13(22)4-5-14(15)21(29)27(2)10-16-19(17(8-23)28(3)26-16)12-6-18(30-11)20(24)25-9-12/h4-7,9,11H,10H2,1-3H3,(H2,24,25)/t11-/m1/s1
IUPAC Name
(16R)-19-amino-13-fluoro-4,8,16-trimethyl-9-oxo-17-oxa-4,5,8,20-tetraazatetracyclo[16.3.1.0^{2,6}.0^{10,15}]docosa-1(22),2,5,10(15),11,13,18,20-octaene-3-carbonitrile
SMILES
C[C@H]1OC2=C(N)N=CC(=C2)C2=C(C#N)N(C)N=C2CN(C)C(=O)C2=C1C=C(F)C=C2

Pharmacology

Indication

Lorlatinib is a third-generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor (TKI) 10 indicated for the treatment of patients with ALK-positive metastatic non-small cell lung cancer (NSCLC) whose disease has progressed on a) the prior use of crizotinib and at least one other ALK inhibitor for metastatic disease, or b) the prior use of alectinib as the first ALK inhibitor therapy for metastatic disease, or c) the prior use of certinib as the first ALK inhibitor therapy for metastatic disease Label.

Associated Conditions
Pharmacodynamics

Based on data from Study B7461001, exposure-response relationships for Grade 3 or 4 hypercholesterolemia and for any Grade 3 or 4 adverse reaction were observed at steady-state exposures achieved at the recommended dosage, with higher probability of the occurrence of adverse reactions with increasing lorlatinib exposure Label.

In 295 patients who received lorlatinib at the recommended dosage of 100 mg once daily and had an ECG measurement in the same Study B7461001, the maximum mean change from baseline for their PR interval was 16.4 ms (2-sided 90% upper confidence interval [CI] 19.4 ms) Label. Among the 284 patients with PR interval <200 ms at baseline, 14% had PR interval prolongation ≥200 ms after starting use with lorlatinib Label. The prolongation of PR interval occurred in a concentration-dependent manner and atrioventricular block occurred in 1% of patients Label.

Finally, in 275 patients who received lorlatinib at the recommended dosage in the activity-estimating portion of Study B7461001, no large mean increases from baseline in the QTcF interval (i.e., >20 ms) were detected Label.

Mechanism of action

Non-small cell lung cancer (NSCLC) accounts for up to 85% of lung cancer cases worldwide and remains a particularly difficult to treat condition 10. The gene rearrangement of anaplastic lymphoma kinase (ALK) is a genetic alteration that drives the development of NSCLC in a number of patients 6,7. Ordinarily, ALK is a natural endogenous tyrosine kinase receptor that plays an important role in the development of the brain and elicits activity on various specific neurons in the nervous system 2,5,6.

Subsequnetly, lorlatinib is a kinase inhibitor with in vitro activity against ALK and number of other tyrosine kinase receptor related targets including ROS1, TYK1, FER, FPS, TRKA, TRKB, TRKC, FAK, FAK2, and ACK Label. Lorlatinib demonstrated in vitro activity against multiple mutant forms of the ALK enzyme, including some mutations detected in tumors at the time of disease progression on crizotinib and other ALK inhibitors Label. Moreover, lorlatinib possesses the capability to cross the blood-brain barrier, allowing it to reach and treat progressive or worsening brain metastases as well 10,5. The overall antitumor activity of lorlatinib in in-vivo models appears to be dose-dependent and correlated with the inhibition of ALK phosphorylation Label.

Although many ALK-positive metastatic NSCLC patients respond to initial tyrosine kinase therapies, such patients also often experience tumor progression 8. Various clinical trials performed with lorlatinib, however, have demonstrated its utility to effect tumor regression in ALK-positive metastatic NSCLC patients who experience tumor progression despite current use or having already used various first and second-generation tyrosine kinase inhibitors like crizotinib, alectinib, or ceritinib 9.

TargetActionsOrganism
AALK tyrosine kinase receptor
inhibitor
Humans
Additional Data Available
Adverse Effects

Comprehensive structured data on known drug adverse effects with statistical prevalence. MedDRA and ICD10 ids are provided for adverse effect conditions and symptoms.

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Additional Data Available
Contraindications

Structured data covering drug contraindications. Each contraindication describes a scenario in which the drug is not to be used. Includes restrictions on co-administration, contraindicated populations, and more.

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Additional Data Available
Blackbox Warnings

Structured data representing warnings from the black box section of drug labels. These warnings cover important and dangerous risks, contraindications, or adverse effects.

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Absorption

The median lorlatinib Tmax was 1.2 hours (0.5 to 4 hours) following a single oral 100 mg dose and 2 hours (0.5 to 23 hours) following 100 mg orally once daily at steady state Label.

The mean absolute bioavailability is 81% (90% CI 75.7%, 86.2%) after oral administration compared to intravenous administration Label.

Administration of lorlatinib with a high fat, high-calorie meal (approximately 1000 calories with 150 calories from protein, 250 calories from carbohydrate, and 500 to 600 calories from fat) had no clinically meaningful effect on lorlatinib pharmacokinetics Label.

Volume of distribution

The mean (CV%) steady-state volume of distribution (Vss) was 305 L (28%) following a single intravenous dose Label.

Protein binding

In vitro, lorlatinib was 66% bound to plasma proteins at a concentration of 2.4 µM Label. The blood-to-plasma ratio was 0.99 Label.

Metabolism

In vitro, lorlatinib is metabolized primarily by CYP3A4 and UGT1A4, with minor contribution from CYP2C8, CYP2C19, CYP3A5, and UGT1A3 Label. In plasma, a benzoic acid metabolite (M8) of lorlatinib resulting from the oxidative cleavage of the amide and aromatic ether bonds of lorlatinib accounted for 21% of the circulating radioactivity in a human [14C] mass balance study Label. The oxidative cleavage metabolite, M8, is pharmacologically inactive Label.

Route of elimination

Following a single oral 100 mg dose of radiolabeled lorlatinib, 48% of the radioactivity was recovered in urine (<1% as unchanged) and 41% in feces (about 9% as unchanged) Label.

Half life

The mean plasma half-life (t½) of lorlatinib was 24 hours (40%) after a single oral 100 mg dose of lorlatinib Label.

Clearance

The mean oral clearance (CL/F) was 11 L/h (35%) following a single oral 100 mg dose and increased to 18 L/h (39%) at steady state, suggesting autoinduction Label.

Toxicity

Although there is no formal data available on the use of lorlatinib in pregnant women, based on findings from animal studies and its mechanism of action, it is believed that lorlatinib can cause embryo-fetal harm when administered to a pregnant woman Label.

There are no data on the presence of lorlatinib or its metabolites in either human or animal milk or its effects on the breastfed infant or on milk production Label. Because of the potential for serious adverse reactions in breastfed infants, instruct women not to breastfeed during treatment with lorlatinib and for 7 days after the final dose Label.

Advise female patients of reproductive potential to use effective non-hormonal contraception during treatment with lorlatinib and for at least 6 months after the final dose Label. Advise females of reproductive potential to use a non-hormonal method of contraception, because lorlatinib can render hormonal contraceptives ineffective Label.

Based on genotoxicity findings, advise males with female partners of reproductive potential to use effective contraception during treatment with lorlatinib and for at least 3 months after the final dose Label.

Based on findings from animal studies, use of lorlatinib may transiently impair male fertility Label.

The safety and effectiveness of lorlatinib in pediatric patients have not been established Label.

Of the 295 patients in Study B7461001 who received 100 mg lorlatinib orally once daily, 18% of patients were aged 65 years or older Label. Although data are limited, no clinically important differences in safety or efficacy were observed between patients aged 65 years or older and younger patients Label.

No dose adjustment is recommended for patients with mild hepatic impairment (total bilirubin ≤ upper limit of normal [ULN] with AST > ULN or total bilirubin >1 to 1.5 × ULN with any AST) Label. The recommended dose of lorlatinib has not been established for patients with moderate or severe hepatic impairment Label.

No dose adjustment is recommended for patients with mild or moderate renal impairment (creatinine clearance [CLcr] 30 to 89 mL/min estimated by Cockcroft-Gault) Label. The recommended dose of lorlatinib has not been established for patients with severe renal impairment Label.

Carcinogenicity studies have not been conducted with lorlatinib Label. Lorlatinib was aneugenic in an in vitro assay in human lymphoblastoid TK6 cells and positive for micronuclei formation in vivo in the bone marrow of rats. Lorlatinib was not mutagenic in an in vitro bacterial reverse mutation (Ames) assay Label.

Dedicated fertility studies were not conducted with lorlatinib Label. Findings in male reproductive organs occurred in repeat-dose toxicity studies and included lower testicular, epididymal, and prostate weights; testicular tubular degeneration/atrophy; prostatic atrophy; and/or epididymal inflammation at 15 mg/kg/day and 7 mg/kg/day in rats and dogs, respectively (approximately 8 and 2 times, respectively, the human exposure at the recommended dose of 100 mg based on AUC) Label. The effects on male reproductive organs were reversible Label.

Distended abdomen, skin rash, and increased cholesterol and triglycerides occurred in animals Label. These findings were accompanied by hyperplasia and dilation of the bile ducts in the liver and acinar atrophy of the pancreas in rats at 15 mg/kg/day and in dogs at 2 mg/kg/day (approximately 8 and 0.5 times, respectively, the human exposure at the recommended dose of 100 mg based on AUC) Label. All effects were reversible within the recovery period Label.

Affected organisms
  • Humans and other mammals
Pathways
Not Available
Pharmacogenomic Effects/ADRs
Not Available

Interactions

Drug Interactions
DrugInteraction
(R)-warfarinThe metabolism of Lorlatinib can be decreased when combined with (R)-warfarin.
(S)-WarfarinThe metabolism of (S)-Warfarin can be decreased when combined with Lorlatinib.
AbataceptThe metabolism of Lorlatinib can be increased when combined with Abatacept.
AbirateroneThe metabolism of Lorlatinib can be decreased when combined with Abiraterone.
AcalabrutinibThe metabolism of Lorlatinib can be decreased when combined with Acalabrutinib.
AcenocoumarolThe metabolism of Lorlatinib can be decreased when combined with Acenocoumarol.
AdalimumabThe metabolism of Lorlatinib can be increased when combined with Adalimumab.
AfelimomabThe metabolism of Lorlatinib can be increased when combined with Afelimomab.
AlbendazoleThe metabolism of Lorlatinib can be decreased when combined with Albendazole.
AlfentanilThe metabolism of Alfentanil can be decreased when combined with Lorlatinib.
Additional Data Available
  • Extended Description
    Extended Description

    Extended description of the mechanism of action and particular properties of each drug interaction.

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  • Severity
    Severity

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  • Evidence Level
    Evidence Level

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  • Action
    Action

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Food Interactions
Not Available

References

Synthesis Reference

Johnson TW, Richardson PF, Bailey S, et al. Discovery of (10R)-7-amino-12-fluoro-2,10,16-trimethyl-15-oxo-10,15,16,17-tetrahydro-2H-8,4-(metheno)pyrazolo[4,3-h][2,5,11]-benzoxadiazacyclotetradecine-3-carbonitrile (PF-06463922), a macrocyclic inhibitor of anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1) with preclinical brain exposure and broad-spectrum potency against ALK-resistant mutations. J Med Chem. 2014;57(11):4720-44.

General References
  1. Shaw AT, Felip E, Bauer TM, Besse B, Navarro A, Postel-Vinay S, Gainor JF, Johnson M, Dietrich J, James LP, Clancy JS, Chen J, Martini JF, Abbattista A, Solomon BJ: Lorlatinib in non-small-cell lung cancer with ALK or ROS1 rearrangement: an international, multicentre, open-label, single-arm first-in-man phase 1 trial. Lancet Oncol. 2017 Dec;18(12):1590-1599. doi: 10.1016/S1470-2045(17)30680-0. Epub 2017 Oct 23. [PubMed:29074098]
  2. Authors unspecified: Lorlatinib in NSCLC: Robust Efficacy Seen. Cancer Discov. 2017 Dec;7(12):1360-1361. doi: 10.1158/2159-8290.CD-NB2017-153. Epub 2017 Nov 3. [PubMed:29101158]
  3. Shaw AT, Friboulet L, Leshchiner I, Gainor JF, Bergqvist S, Brooun A, Burke BJ, Deng YL, Liu W, Dardaei L, Frias RL, Schultz KR, Logan J, James LP, Smeal T, Timofeevski S, Katayama R, Iafrate AJ, Le L, McTigue M, Getz G, Johnson TW, Engelman JA: Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. N Engl J Med. 2016 Jan 7;374(1):54-61. doi: 10.1056/NEJMoa1508887. Epub 2015 Dec 23. [PubMed:26698910]
  4. Authors unspecified: Lorlatinib Is Active in Drug-Resistant NSCLC. Cancer Discov. 2016 Aug;6(8):OF1. doi: 10.1158/2159-8290.CD-NB2016-087. Epub 2016 Jul 8. [PubMed:27401797]
  5. Collier TL, Maresca KP, Normandin MD, Richardson P, McCarthy TJ, Liang SH, Waterhouse RN, Vasdev N: Brain Penetration of the ROS1/ALK Inhibitor Lorlatinib Confirmed by PET. Mol Imaging. 2017 Jan-Dec;16:1536012117736669. doi: 10.1177/1536012117736669. [PubMed:29067878]
  6. Chiarle R, Voena C, Ambrogio C, Piva R, Inghirami G: The anaplastic lymphoma kinase in the pathogenesis of cancer. Nat Rev Cancer. 2008 Jan;8(1):11-23. doi: 10.1038/nrc2291. [PubMed:18097461]
  7. Guerin A, Sasane M, Zhang J, Macalalad AR, Galebach P, Jarvis J, Kageleiry A, Culver K, Wu EQ, Wakelee H: ALK rearrangement testing and treatment patterns for patients with ALK-positive non-small cell lung cancer. Cancer Epidemiol. 2015 Jun;39(3):307-12. doi: 10.1016/j.canep.2015.04.005. Epub 2015 Apr 23. [PubMed:25914136]
  8. Lin JJ, Riely GJ, Shaw AT: Targeting ALK: Precision Medicine Takes on Drug Resistance. Cancer Discov. 2017 Feb;7(2):137-155. doi: 10.1158/2159-8290.CD-16-1123. Epub 2017 Jan 25. [PubMed:28122866]
  9. Waqar SN, Morgensztern D: Lorlatinib: a new-generation drug for ALK-positive NSCLC. Lancet Oncol. 2018 Dec;19(12):1555-1557. doi: 10.1016/S1470-2045(18)30789-7. Epub 2018 Nov 6. [PubMed:30413381]
  10. FDA Approval of [Link]
External Links
PubChem Compound
71731823
PubChem Substance
347828429
ChemSpider
32813339
BindingDB
50018830
ChEBI
143117
ChEMBL
CHEMBL3286830
HET
5P8
Wikipedia
Lorlatinib
ATC Codes
L01XE44 — Lorlatinib
PDB Entries
4cli / 4clj / 4uxl / 5a9u / 5aa8 / 5aa9
FDA label
Download (530 KB)
MSDS
Download (22.3 KB)

Clinical Trials

Clinical Trials
PhaseStatusPurposeConditionsCount
1CompletedBasic ScienceHealthy Volunteers1
1CompletedOtherHealthy Volunteers1
1Not Yet RecruitingTreatmentAdults / Drug Drug Interaction (DDI) / Healthy Volunteers / Humans1
1RecruitingBasic ScienceHealthy Volunteers1
1RecruitingOtherImpaired Renal Function1
1RecruitingTreatmentAdvanced Cancers1
1RecruitingTreatmentNeuroblastomas1
2Active Not RecruitingTreatmentALK-positive Non Small Cell Lung Cancer (NSCLC) and ROS1-positive NSCLC1
2Active Not RecruitingTreatmentLung Cancer Non-Small Cell Cancer (NSCLC)1
2Not Yet RecruitingTreatmentLung Cancer Non-Small Cell Cancer (NSCLC)1
2RecruitingScreeningALK Gene Rearrangement / ALK positive / Lung Non-Squamous Non-Small Cell Carcinoma / Non-Squamous Non-Small Cell Lung Carcinoma / Stage IV Lung Cancer AJCC v8 / Stage IVA Lung Cancer AJCC v8 / Stage IVB Lung Cancer AJCC v81
2RecruitingTreatmentAnaplastic Large Cell Lymphoma, ALK-Positive1
2RecruitingTreatmentLung Cancer Non-Small Cell Cancer (NSCLC)3
3RecruitingTreatmentLung Cancer Non-Small Cell Cancer (NSCLC)1
Not AvailableNo Longer AvailableNot AvailableNon Small Cell Lung Cancer ALK Positive or ROS1 Positive / Non Small Cell Lung Cancer Harboring Molecular Alterations / Non Small Cell Lung Cancer With ALK or ROS1 Rearrangement1

Pharmacoeconomics

Manufacturers
Not Available
Packagers
Not Available
Dosage forms
FormRouteStrength
TabletOral100 mg
TabletOral25 mg
Tablet, film coatedOral100 mg/1
Tablet, film coatedOral25 mg/1
Prices
Not Available
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)
US8680111No2014-03-252033-03-05Us
Additional Data Available
  • Filed On
    Filed On

    The date on which a patent was filed with the relevant government.

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Properties

State
Solid
Experimental Properties
Not Available
Predicted Properties
PropertyValueSource
Water Solubility0.108 mg/mLALOGPS
logP2.01ALOGPS
logP1.63ChemAxon
logS-3.6ALOGPS
pKa (Strongest Acidic)19.7ChemAxon
pKa (Strongest Basic)5.71ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count6ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area110.06 Å2ChemAxon
Rotatable Bond Count0ChemAxon
Refractivity121.17 m3·mol-1ChemAxon
Polarizability40.42 Å3ChemAxon
Number of Rings4ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Predicted ADMET features
Not Available

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted GC-MS Spectrum - GC-MSPredicted GC-MSNot Available
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSNot Available

Taxonomy

Description
This compound belongs to the class of organic compounds known as macrolactams. These are cyclic amides of amino carboxylic acids, having a 1-azacycloalkan-2-one structure, or analogues having unsaturation or heteroatoms replacing one or more carbon atoms of the ring. They are nitrogen analogues (the a nitrogen atom replacing the o atom of the cyclic carboxylic acid group ) of the naturally occurring macrolides.
Kingdom
Organic compounds
Super Class
Phenylpropanoids and polyketides
Class
Macrolactams
Sub Class
Not Available
Direct Parent
Macrolactams
Alternative Parents
Pyrazolylpyridines / Alkyl aryl ethers / Aminopyridines and derivatives / Aryl fluorides / Benzenoids / Imidolactams / Tertiary carboxylic acid amides / Pyrazoles / Heteroaromatic compounds / Amino acids and derivatives
show 8 more
Substituents
Macrolactam / 3-pyrazolylpyridine / Alkyl aryl ether / Aminopyridine / Aryl fluoride / Aryl halide / Imidolactam / Benzenoid / Pyridine / Azole
show 25 more
Molecular Framework
Aromatic heteropolycyclic compounds
External Descriptors
Not Available

Targets

Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
Transmembrane receptor protein tyrosine kinase activity
Specific Function
Neuronal orphan receptor tyrosine kinase that is essentially and transiently expressed in specific regions of the central and peripheral nervous systems and plays an important role in the genesis a...
Gene Name
ALK
Uniprot ID
Q9UM73
Uniprot Name
ALK tyrosine kinase receptor
Molecular Weight
176440.535 Da

Enzymes

Kind
Protein group
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
Inhibitor
Inducer
General Function
Vitamin d3 25-hydroxylase activity
Specific Function
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation react...

Components:
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
General Function
Oxygen binding
Specific Function
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...
Gene Name
CYP3A5
Uniprot ID
P20815
Uniprot Name
Cytochrome P450 3A5
Molecular Weight
57108.065 Da
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Inducer
General Function
Steroid hydroxylase activity
Specific Function
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...
Gene Name
CYP2B6
Uniprot ID
P20813
Uniprot Name
Cytochrome P450 2B6
Molecular Weight
56277.81 Da
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
General Function
Steroid hydroxylase activity
Specific Function
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...
Gene Name
CYP2C8
Uniprot ID
P10632
Uniprot Name
Cytochrome P450 2C8
Molecular Weight
55824.275 Da
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
General Function
Steroid hydroxylase activity
Specific Function
Responsible for the metabolism of a number of therapeutic agents such as the anticonvulsant drug S-mephenytoin, omeprazole, proguanil, certain barbiturates, diazepam, propranolol, citalopram and im...
Gene Name
CYP2C19
Uniprot ID
P33261
Uniprot Name
Cytochrome P450 2C19
Molecular Weight
55930.545 Da
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Substrate
General Function
Retinoic acid binding
Specific Function
UDPGT is of major importance in the conjugation and subsequent elimination of potentially toxic xenobiotics and endogenous compounds. Isoform 2 lacks transferase activity but acts as a negative reg...
Gene Name
UGT1A3
Uniprot ID
P35503
Uniprot Name
UDP-glucuronosyltransferase 1-3
Molecular Weight
60337.835 Da

Drug created on October 20, 2016 15:24 / Updated on July 13, 2019 00:58