Vemurafenib

Identification

Summary

Vemurafenibis a kinase inhibitor used to treat patients with Erdheim-Chester Disease who have the BRAF V600 mutation, and melanoma in patients who have the BRAF V600E mutation.

Brand Names

Zelboraf

Generic Name

Vemurafenib

DrugBank Accession Number

DB08881

Background

Vemurafenib is a competitive kinase inhibitor with activity against BRAF kinase with mutations like V600E.²It exerts its function by binding to the ATP-binding domain of the mutant BRAF.³Vemurafenib was co-developed by Roche and Plexxikon and it obtained its FDA approval on August 17, 2011, under the company Hoffmann La Roche. After approval, Roche in collaboration with Genentech launched a broad development program.⁸

Type

Small Molecule

Groups

Approved

Structure

3D

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MOL SDF 3D-SDF PDB SMILES InChI

Similar Structures

Structure for Vemurafenib (DB08881)

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Weight

Average: 489.922
Monoisotopic: 489.072546264

Chemical Formula

C₂₃H₁₈ClF₂N₃O₃S

Synonyms

• Vemurafenib
• Vémurafénib
• Vemurafenibum

External IDs

• PLX-4032
• PLX4032
• RG-7204
• RG7204
• RO-51-85426
• RO-5185426
• RO5185426

Pharmacology

Indication

Vemurafenib is approved since 2011 for the treatment of metastatic melanoma with a mutation on BRAF in the valine located in the exon 15 at codon 600, this mutation is denominated as V600E.³The V600E mutation, a substitution of glutamic acid for valine, accounts for 54% of the cases of cutaneous melanoma.⁴Vemurafenib approval was extended in 2017, for its use as a treatment of adult patients with Erdheim-Chester Disease whose cancer cells present BRAF V600 mutation.⁹Erdheim-Chester disease is an extremely rare histiocyte cell disorder that affects large bones, large vessels, central nervous system, as well as, skin and lungs. It is reported an association of Erdheim-Chester disease and V600E mutation.⁵

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Associated Conditions

• Metastatic Melanoma
• Refractory Lung Non-Small Cell Carcinoma
• Unresectable Melanoma
• Refractory Erdheim-Chester disease

Contraindications & Blackbox Warnings

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Pharmacodynamics

BRAF activation results in cell growth, proliferation, and metastasis. BRAF is an intermediary molecule in MAPK whose activation depends on ERK activation, elevation of cyclin D1 and cellular proliferation. The mutation V600E produces a constitutively form of BRAF. Vemurafenib has been shown to reduce all activation markers related to BRAF; in clinical trials, vemurafenib treatment showed a reduction of cytoplasmic phosphorylated ERK and a cell proliferation driven by Ki-67. Studies also reported decrease in MAPK-related metabolic activity.³All the different reports indicate thet Vemurafenib generates an almost complete inhibition of the MAPK pathway.

Mechanism of action

Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase. Vemurafenif is a small molecule that interacts as a competitive inhibitor of the mutated species of BRAF. It is especially potent against the BRAF V600E mutation. Vemurafenib blocks downstream processes to inhibit tumour growth and eventually trigger apoptosis. Vemurafenib does not have antitumour effects against melanoma cell lines with the wild-type BRAF mutation.¹⁰

Target	Actions	Organism
ASerine/threonine-protein kinase B-raf	inhibitor	Humans

Absorption

Vemurafenib is well absorbed after oral administration.⁶Peak concentrations are reached in 3 hours when an oral dose of 960 mg twice daily for 15 days has been given to patients. In the same conditions, Vemurafenib presents a Cmax of 62 mcg/ml and AUC of 601 mcg h/ml.^LabelIt is unknown how food affects the absorption of vemurafenib. It presents an accumulation ratio of 7.36 after repeating doses of 960 mg¹⁰

Volume of distribution

The estimation of the volume of distribution for Vemurafenib is 106 L.⁷

Protein binding

Vemurafenib highly binds to plasma proteins where >99% of the administered dose will be found protein bound to serum albumin and alpha-1 acid glycoprotein.⁷

Metabolism

Vemurafenib is metabolized by CYP3A4 and the metabolites make up 5% of the components in plasma. The parent compound makes up for the remaining 95%.⁷

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• Vemurafenib
  • vemurafenib intermediary metabolite
    • secondary metabolite of vemurafenib alternative
    • secondary metabolite of vemurafenib

Route of elimination

Analysis showed that 94% of administered Vemurafenib is excreted via feces and 1% is excreted by urine.⁷

Half-life

The elimination half-life of Vemurafenib is estimated to be 57 hours (range of 30-120 hours).⁷

间隙

The total body clearance is 31 L/day.⁷

Adverse Effects

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Toxicity

In the few toxicity reports, it has been shown an increased in the development of cutaneous squamous cell carcinomas or acceleration in pre-existant tumor growth.^Label

Pathways

Not Available

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Not Available

Interactions

Drug InteractionsLearn More" title="" id="structured-interactions-info" class="drug-info-popup" href="javascript:void(0);">

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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Abametapir	The serum concentration of Vemurafenib can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Vemurafenib can be increased when combined with Abatacept.
Abemaciclib	The serum concentration of Abemaciclib can be increased when it is combined with Vemurafenib.
Abrocitinib	The serum concentration of Vemurafenib can be increased when it is combined with Abrocitinib.
Acalabrutinib	The metabolism of Acalabrutinib can be increased when combined with Vemurafenib.
Acarbose	The therapeutic efficacy of Acarbose can be increased when used in combination with Vemurafenib.
Acebutolol	The metabolism of Acebutolol can be decreased when combined with Vemurafenib.
Acenocoumarol	The serum concentration of Acenocoumarol can be increased when it is combined with Vemurafenib.
Acetaminophen	The serum concentration of Acetaminophen can be increased when it is combined with Vemurafenib.
Acetazolamide	The metabolism of Vemurafenib can be decreased when combined with Acetazolamide.

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Food Interactions

• Do not take with or immediately after a high-fat meal. Taking vemurafenib with a high-fat meal may increase the AUC and Cmax by approximately 5 fold and 2.5 fold, respectively.
• Exercise caution with grapefruit products. Grapefruit inhibits the CYP3A4 metabolism of vemurafenib, which may increase its serum concentration.
• Exercise caution with St. John's Wort. This herb induces the CYP3A4 metabolism of vemurafenib and may reduce its serum concentration.
• Limit caffeine intake. Vemurafenib inhibits CYP1A2, which may increase the serum levels and adverse effects of caffeine.
• Take with or without food.

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Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Zelboraf	Tablet, film coated	240 mg	Oral	Roche Registration Gmb H	2016-09-08	Not applicable
Zelboraf	Tablet	240 mg	Oral	Hoffmann La Roche	2012-03-05	Not applicable
Zelboraf	Tablet, film coated	240 mg/1	Oral	Genentech, Inc.	2011-08-17	Not applicable

Categories

ATC Codes

G01AE10 — Combinations of sulfonamides

• G01AE — Sulfonamides
• G01A — ANTIINFECTIVES AND ANTISEPTICS, EXCL. COMBINATIONS WITH CORTICOSTEROIDS
• G01 — GYNECOLOGICAL ANTIINFECTIVES AND ANTISEPTICS
• G — GENITO URINARY SYSTEM AND SEX HORMONES

L01EC01 — Vemurafenib

• L01EC — B-Raf serine-threonine kinase (BRAF) inhibitors
• L01E — PROTEIN KINASE INHIBITORS
• L01 — ANTINEOPLASTIC AGENTS
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Amides
• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• B-Raf serine-threonine kinase (BRAF) inhibitors
• BCRP/ABCG2 Inhibitors
• BCRP/ABCG2 Substrates
• Cytochrome P-450 CYP1A2 Inhibitors
• Cytochrome P-450 CYP1A2 Inhibitors (moderate)
• Cytochrome P-450 CYP2B6 Inducers
• Cytochrome P-450 CYP2B6 Inducers (strength unknown)
• Cytochrome P-450 CYP2C8 Inhibitors
• Cytochrome P-450 CYP2C8 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2C9 Inhibitors
• Cytochrome P-450 CYP2C9 Inhibitors (strength unknown)
• Cytochrome P-450 CYP2D6 Inhibitors
• Cytochrome P-450 CYP2D6 Inhibitors (weak)
• Cytochrome P-450 CYP3A Inducers
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Inducers
• Cytochrome P-450 CYP3A4 Inducers (strength unknown)
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 CYP3A4 Substrates with a Narrow Therapeutic Index
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Drugs causing inadvertant photosensitivity
• Enzyme Inhibitors
• Genito Urinary System and Sex Hormones
• Gynecological Antiinfectives and Antiseptics
• Heterocyclic Compounds, Fused-Ring
• Highest Risk QTc-Prolonging Agents
• Indoles
• Kinase Inhibitor
• Narrow Therapeutic Index Drugs
• P-glycoprotein inhibitors
• P-glycoprotein substrates
• P-glycoprotein substrates with a Narrow Therapeutic Index
• Photosensitizing Agents
• Protein Kinase Inhibitors
• QTc Prolonging Agents
• Sulfonamides
• Sulfones
• Sulfur Compounds
• Tyrosine Kinase Inhibitors

Chemical TaxonomyProvided byClassyfire

Description

This compound belongs to the class of organic compounds known as aryl-phenylketones. These are aromatic compounds containing a ketone substituted by one aryl group, and a phenyl group.

Kingdom

Organic compounds

Super Class

Organic oxygen compounds

Class

Organooxygen compounds

Sub Class

Carbonyl compounds

Direct Parent

Aryl-phenylketones

Alternative Parents

Phenylpyridines/Sulfanilides/Pyrrolopyridines/Benzoyl derivatives/Chlorobenzenes/Fluorobenzenes/Organosulfonamides/Organic sulfonamides/Aryl chlorides/Aryl fluorides /Substituted pyrroles/Heteroaromatic compounds/Aminosulfonyl compounds/Vinylogous halides/Vinylogous amides/Azacyclic compounds/Organopnictogen compounds/Organonitrogen compounds/Organofluorides/Organochlorides/Organic oxides/Hydrocarbon derivatives

show 12 more

Substituents

3-phenylpyridine/Aminosulfonyl compound/Aromatic heteropolycyclic compound/Aryl chloride/Aryl fluoride/Aryl halide/Aryl-phenylketone/Azacycle/Benzenoid/Benzoyl /Chlorobenzene/Fluorobenzene/Halobenzene/Heteroaromatic compound/Hydrocarbon derivative/Monocyclic benzene moiety/Organic nitrogen compound/Organic oxide/Organic sulfonic acid amide/Organic sulfonic acid or derivatives/Organochloride/Organofluoride/Organohalogen compound/Organoheterocyclic compound/Organonitrogen compound/Organopnictogen compound/Organosulfonic acid amide/Organosulfonic acid or derivatives/Organosulfur compound/Pyridine/Pyrrole/Pyrrolopyridine/Substituted pyrrole/Sulfanilide/Sulfonyl/Vinylogous amide/Vinylogous halide

show 27 more

Molecular Framework

Aromatic heteropolycyclic compounds

External Descriptors

organofluorine compound, sulfonamide, organochlorine compound, pyrrolopyridine (CHEBI:63637)

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

207SMY3FQT

CAS number

918504-65-1

InChI Key

GPXBXXGIAQBQNI-UHFFFAOYSA-N

InChI

InChI=1S/C23H18ClF2N3O3S/c1-2-9-33(31,32)29-19-8-7-18(25)20(21(19)26)22(30)17-12-28-23-16(17)10-14(11-27-23)13-3-5-15(24)6-4-13/h3-8,10-12,29H,2,9H2,1H3,(H,27,28)

IUPAC Name

N-{3-[5-(4-chlorophenyl)-1H-pyrrolo[2,3-b]pyridine-3-carbonyl]-2,4-difluorophenyl}propane-1-sulfonamide

SMILES

CCCS(=O)(=O)NC1=C(F)C(C(=O)C2=CNC3=NC=C(C=C23)C2=CC=C(Cl)C=C2)=C(F)C=C1

References

一般引用

1. Jordan EJ, Kelly CM: Vemurafenib for the treatment of melanoma. Expert Opin Pharmacother. 2012 Dec;13(17):2533-43. doi: 10.1517/14656566.2012.737780. Epub 2012 Oct 24. [Article]
2. Kim G, McKee AE, Ning YM, Hazarika M, Theoret M, Johnson JR, Xu QC, Tang S, Sridhara R, Jiang X, He K, Roscoe D, McGuinn WD, Helms WS, Russell AM, Miksinski SP, Zirkelbach JF, Earp J, Liu Q, Ibrahim A, Justice R, Pazdur R: FDA approval summary: vemurafenib for treatment of unresectable or metastatic melanoma with the BRAFV600E mutation. Clin Cancer Res. 2014 Oct 1;20(19):4994-5000. doi: 10.1158/1078-0432.CCR-14-0776. Epub 2014 Aug 5. [Article]
3. Luke JJ, Hodi FS: Vemurafenib and BRAF inhibition: a new class of treatment for metastatic melanoma. Clin Cancer Res. 2012 Jan 1;18(1):9-14. doi: 10.1158/1078-0432.CCR-11-2197. Epub 2011 Nov 14. [Article]
4. Schirosi L, Strippoli S, Gaudio F, Graziano G, Popescu O, Guida M, Simone G, Mangia A: Is immunohistochemistry of BRAF V600E useful as a screening tool and during progression disease of melanoma patients? BMC Cancer. 2016 Nov 18;16(1):905. [Article]
5. Stempel JM, Bustamante Alvarez JG, Carpio AM, Mittal V, Dourado C: Erdheim-Chester disease, moving away from the orphan diseases: A case report. Respir Med Case Rep. 2016 Dec 3;20:55-58. eCollection 2017. [Article]
6. Zhang W, Heinzmann D, Grippo JF: Clinical Pharmacokinetics of Vemurafenib. Clin Pharmacokinet. 2017 Mar 2. doi: 10.1007/s40262-017-0523-7. [Article]
7. Goldinger SM, Rinderknecht J, Dummer R, Kuhn FP, Yang KH, Lee L, Ayala RC, Racha J, Geng W, Moore D, Liu M, Joe AK, Bazan SP, Grippo JF: A single-dose mass balance and metabolite-profiling study of vemurafenib in patients with metastatic melanoma. Pharmacol Res Perspect. 2015 Mar;3(2):e00113. doi: 10.1002/prp2.113. [Article]
8. Roche news [Link]
9. FDA News and Events [Link]
10. FDA Vemurafenib application [Link]

External Links

KEGG Drug

D09996

PubChem Compound

42611257

PubChem Substance

175427131

ChemSpider

24747352

BindingDB

50396483

RxNav

1147220

ChEBI

63637

ChEMBL

CHEMBL1229517

ZINC

ZINC000052509366

PharmGKB

PA165946873

PDBe Ligand

032

RxList

RxList Drug Page

Drugs.com

Drugs.com Drug Page

Wikipedia

Vemurafenib

PDB Entries

3og7/4rzv/5hes

FDA label

Download (304 KB)

MSDS

Download (51 KB)

Clinical Trials

Clinical TrialsLearn More" title="" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">

Phase	Status	Purpose	Conditions	Count
4	Completed	Treatment	Melanoma, Malignant	1
4	Completed	Treatment	Neoplasm	1
4	Terminated	Other	Metastatic Melanoma	1
3	Active Not Recruiting	Treatment	Melanoma	2
3	Completed	Treatment	Melanoma	2
3	Completed	Treatment	Melanoma, Malignant	3
3	Recruiting	Treatment	Colorectal Cancer	1
3	Withdrawn	Treatment	Melanoma	1
2	Active Not Recruiting	Treatment	Advanced Malignant Solid Tumor/Ann Arbor Stage III Childhood Non-Hodgkin Lymphoma/Ann Arbor Stage IV Childhood Non-Hodgkin Lymphoma/Ependymoma/Ewing's Sarcoma/Hepatoblastomas/Langerhans Cell Histiocytosis (LCH)/Malignant Germ Cell Neoplasm/Malignant Glioma/Osteosarcoma/Peripheral Primitive Neuroectodermal Tumor/Recurrent Childhood Central Nervous System Neoplasm/Recurrent Childhood Non-Hodgkin Lymphoma/Recurrent Malignant Solid Neoplasm/Recurrent Neuroblastoma/Refractory Malignant Solid Neoplasm/Refractory Neuroblastoma/Refractory Non-Hodgkin's lymphoma/Refractory, primary Central Nervous System Neoplasm/Rhabdoid Tumors/Rhabdomyosarcomas/Soft Tissue Sarcoma/Wilms' tumor	1
2	Active Not Recruiting	Treatment	Anaplastic Thyroid Carcinoma/转移性甲状腺癌/Poorly differentiated thyroid carcinoma/Stage IVA Thyroid Gland Anaplastic Carcinoma AJCC v8/Stage IVB Thyroid Gland Anaplastic Carcinoma AJCC v8/Stage IVC Thyroid Gland Anaplastic Carcinoma AJCC v8/Unresectable Thyroid Gland Carcinoma	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet	Oral	240 mg
Tablet, film coated	Oral
Tablet, film coated	Oral	240 mg/1
Tablet, film coated	Oral	240 mg

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US8470818	No	2013-06-25	2026-08-02
US8143271	No	2012-03-27	2026-06-21
US7863288	No	2011-01-04	2029-06-20
US7504509	No	2009-03-17	2026-10-22
US8741920	No	2014-06-03	2030-07-27
US9447089	No	2016-09-20	2032-06-06

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	272°C	MSDS
water solubility	<1 mg/mL	MSDS
logP	5.1	MSDS
Caco2 permeability	2.9E-06	FDA review
pKa	7.1	Royal Soc Chem

Predicted Properties

Property	Value	Source
Water Solubility	0.000362 mg/mL	ALOGPS
logP	4.95	ALOGPS
logP	4.62	Chemaxon
logS	-6.1	ALOGPS
pKa (Strongest Acidic)	8.87	Chemaxon
pKa (Strongest Basic)	2.3	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	4	Chemaxon
Hydrogen Donor Count	2	Chemaxon
Polar Surface Area	91.92 Å2	Chemaxon
Rotatable Bond Count	6	Chemaxon
Refractivity	121.97 m3·mol-1	Chemaxon
Polarizability	48.1 Å3	Chemaxon
Number of Rings	4	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like规则	Yes	Chemaxon

Predicted ADMET Features

Property	Value	Probability
Human Intestinal Absorption	+	1.0
Blood Brain Barrier	+	0.745
Caco-2 permeable	-	0.6222
P-glycoprotein substrate	Non-substrate	0.6215
P-glycoprotein inhibitor I	Non-inhibitor	0.5884
P-glycoprotein inhibitor II	Non-inhibitor	0.699
Renal organic cation transporter	Non-inhibitor	0.864
CYP450 2C9 substrate	Non-substrate	0.7628
CYP450 2D6 substrate	Non-substrate	0.8038
CYP450 3A4 substrate	Substrate	0.5645
CYP450 1A2 substrate	Inhibitor	0.5762
CYP450 2C9 inhibitor	Inhibitor	0.5987
CYP450 2D6 inhibitor	Non-inhibitor	0.7329
CYP450 2C19 inhibitor	Inhibitor	0.6508
CYP450 3A4 inhibitor	Inhibitor	0.7061
CYP450 inhibitory promiscuity	High CYP Inhibitory Promiscuity	0.9553
Ames test	Non AMES toxic	0.6323
Carcinogenicity	Non-carcinogens	0.7229
Biodegradation	Not ready biodegradable	1.0
Rat acute toxicity	2.5179 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.6688
hERG inhibition (predictor II)	Non-inhibitor	0.5302

ADMET data is predicted usingadmetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
预测MS / MS谱- 20 v,正面(注释d)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	Not Available
MS/MS Spectrum - , positive	LC-MS/MS	splash10-0006-0024900000-4911e6c7ad52fd2c2896

Targets

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Binding Properties

×

Property	Measurement	pH	Temperature (°C)	References
IC 50 (nM)	100	N/A	N/A	A28071

Details

Binding Properties 1.Serine/threonine-protein kinase B-raf

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

Protein serine/threonine kinase activity

Specific Function

Protein kinase involved in the transduction of mitogenic signals from the cell membrane to the nucleus. May play a role in the postsynaptic responses of hippocampal neuron. Phosphorylates MAP2K1, a...

Gene Name

BRAF

Uniprot ID

P15056

Uniprot Name

Serine/threonine-protein kinase B-raf

分子量

84436.135 Da

References

1. Jordan EJ, Kelly CM: Vemurafenib for the treatment of melanoma. Expert Opin Pharmacother. 2012 Dec;13(17):2533-43. doi: 10.1517/14656566.2012.737780. Epub 2012 Oct 24. [Article]

×

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Drug created at May 20, 2013 06:41 / Updated at April 30, 2023 03:04