Tirbanibulin

Identification

Summary

Tirbanibulin is a tyrosine kinase and tubulin inhibitor used to treat actinic keratosis on the face or scalp.

Brand Names

Klisyri

Generic Name

Tirbanibulin

DrugBank Accession Number

DB06137

Background

Tirbanibulin (KX-O1 or KX2–391) is a dual inhibitor of Src Kinase and tubulin.⁴ On December 14, 2020, tirbanibulin was approved by the FDA for the topical treatment of actinic keratosis on the face or scalp. It is marketed under the brand name Klisyri.¹² Actinic keratosis is a chronic condition characterized by lesions, which can potentially transform into invasive squamous cell carcinoma with a risk of 1% over 10 years.^3,7 Tirbanibulin blocks the molecular pathways that promote the proliferation, survival, and metastasis of malignant cells. Tirbanibulin exhibits antitumour effects in vitro and in vivo ⁹ and has been investigated for its antitumor efficacy in the management of various cancers, such as prostate cancer and breast cancer.^4,5,6

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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Similar Structures

Structure for Tirbanibulin (DB06137)

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Weight

Average: 431.536
Monoisotopic: 431.220891806

Chemical Formula

C₂₆H₂₉N₃O₃

Synonyms

• Tirbanibulin

External IDs

• KX-01
• KX-2-391
• KX-2391
• KX2-391

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Pharmacology

Indication

Tirbanibulin is indicated for the topical treatment of actinic keratosis on the face or scalp.¹¹

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Treatment of	Actinic keratoses of the face		••••••••••••			••••••••
Treatment of	Actinic keratoses of the scalp		••••••••••••			••••••••

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Pharmacodynamics

In clinical trials composed comprising patients with actinic keratosis of the face or scalp, tirbanibulin promoted complete clearance of actinic keratosis lesions at day 57 in treated areas in 44-54% of patients compared to 5-13% of patients who received the placebo.¹¹ Actinic keratosis is a chronic, pre-malignant condition characterized by lesions and proliferation of neoplastic keratinocytes.³ Tirbanibulin mediates an anti-proliferative effect by inhibiting tubulin polymerization and Src kinase signalling.¹

Tirbanibulin inhibited primary tumour growth and metastasis in many preclinical animal models of cancer.^2,4,5,6 In human triple-negative breast cancer, or estrogen receptor (ER)/progesterone receptor (PR)/human epidermal growth factor receptor 2 (HER2)-negative tumour, xenografts, tirbanibulin suppressed tumour growth and metastasis.⁴ Tirbanibulin was also shown to restore functional ERα expression in ERα-negative breast tumours.¹⁰ Tirbanibulin promoted synergistic tumour growth inhibition of breast cancer cell lines when used in combination with tamoxifen ^5,10 and paclitaxel.⁴

In a clinical trial comprising patients with advanced solid tumours, dose-limiting toxicities of tirbanibulin included elevated liver transaminases, neutropenia and fatigue.⁶

Mechanism of action

Src tyrosine kinases regulate normal cell growth: the expression of Src kinase is upregulated during the normal hair cycle during the proliferative anagen phase. Additionally, Src tyrosine kinases act as key modulators of cancer cell proliferation, survival, angiogenesis, migration, invasion and metastasis. Src is frequently upregulated in various epithelial tumours including colon, breast and pancreas compared with the adjacent normal tissues. The expression and activity of Src are also enhanced in human actinic keratosis, which is characterized by hyperproliferative premalignant skin lesions.⁸ The pathogenesis of actinic keratosis commonly involves skin inflammation, oxidative stress, immunosuppression, impaired apoptosis, mutagenesis, dysregulation of keratinocyte growth and proliferation, and tissue remodelling.⁷ In vitro studies suggest that Src plays a predominant role in the early stages of human skin tumour development, rather than at later stages of tumour progression.⁸

The exact mechanism of tirbanibulin as a topical treatment of actinic keratosis has not been fully elucidated;¹¹ however, it mainly works by inhibiting fast proliferating cells.³ Tirbanibulin is a non-ATP competitive Src kinase inhibitor and tubulin polymerization inhibitor. It binds to the peptide substrate binding site of Src, a primary target of tirbanibulin, and blocking its downstream signalling pathways that promote cancer cell migration, proliferation, and survival.^3,5 Tublin is responsible for cell migration, protein transport, and mitosis: tibranibulin directly binds to the colchicine-binding site of beta-tubulin and causes induces tubulin depolymerization.² It is also hypothesized that inhibition of Src can also contribute to the inhibitory effects on microtubule polymerization.⁹ At low nanomolar concentrations, tirbanibulin induces G2/M phase cell cycle arrest in a reversible ^2,5 and dose-dependent manner. By inhibiting microtubule polymerization, tirbanibulin also induces mitotic catastrophe.⁹

Target	Actions	Organism
ATubulin beta chain	inhibitor	Humans
AProto-oncogene tyrosine-protein kinase Src	inhibitor	Humans

Absorption

Tirbanibulin demonstrates good oral bioavailability.² Following topical administration of doses ranging from 54 to 295 mg on the face or scalp, the steady-state concentration of tirbanibulin was achieved by 72 hours. At five days following initial administration, the mean C_max was 0.34±0.30 ng/mL in subjects who received topical treatment on the face and 0.18±0.10 ng/mL in subjects who received topical treatment on the scalp. The mean AUC₂₄ was 5.0±3.9 h x ng/mL in subjects who received topical treatment on the face and 3.2±1.9 h x ng/mL in subjects who received topical treatment on the scalp. The median T_max was about seven hours.¹¹

Volume of distribution

There is limited information on the volume of distribution of tirbanibulin. In mouse HT29 xenograft studies, the tissue to plasma ration of tirbanibulin was 1.52.⁶

Protein binding

Tirbanibulin is 88% bound to plasma proteins and the extent of plasma protein binding is independent of drug concentrations in the range of 0.01 to 10 µg/mL.¹¹

Metabolism

In vitro, tirbanibulin is mainly metabolized by CYP3A4, and to a lesser extent, CYP2C8. In adult subjects with actinic keratosis, detected metabolites were KX2-5036 and KX2-5163, which were pharmacologically inactive metabolites with the highest plasma concentrations of 0.09 ng/mL and 0.12 ng/mL, respectively.¹¹

Route of elimination

There is limited information on the route of elimination of tirbanibulin.

Half-life

The half-life is about 4 hours.⁶

Clearance

There is limited information on the clearance rate of tirbanibulin.

Adverse Effects

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Toxicity

The LD₅₀ value of tirbanibulin has not been determined. While there is limited information on overdose from tirbanibulin, it may lead to an increase in the incidence and severity of local skin reactions.¹¹

Pathways

Not Available

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Not Available

Interactions

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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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Etrasimod	The risk or severity of immunosuppression can be increased when Tirbanibulin is combined with Etrasimod.
Voriconazole	The serum concentration of Tirbanibulin can be increased when it is combined with Voriconazole.

Food Interactions

No interactions found.

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Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Klisyri	Ointment	10 mg/1g	Topical	Almirall, LLC	2020-12-14	Not applicable
Klisyri	Ointment	10 mg/g	Cutaneous	Almirall, S.A.	2021-10-06	Not applicable
Onakta	Ointment	1 % w/w	Topical	Avir Pharma Inc.	Not applicable	Not applicable

Categories

ATC Codes

D06BX03 — Tirbanibulin

• D06BX — Other chemotherapeutics
• D06B — CHEMOTHERAPEUTICS FOR TOPICAL USE
• D06 — ANTIBIOTICS AND CHEMOTHERAPEUTICS FOR DERMATOLOGICAL USE
• D — DERMATOLOGICALS

Drug Categories

• Acetates
• Acids, Acyclic
• Amides
• Antineoplastic Agents
• Cytochrome P-450 CYP1A2 Inhibitors
• Cytochrome P-450 CYP1A2 Inhibitors (weak)
• Cytochrome P-450 CYP2B6 Inhibitors
• Cytochrome P-450 CYP2B6 Inhibitors (weak)
• Cytochrome P-450 CYP2C19 Inhibitors
• Cytochrome P-450 CYP2C19 Inhibitors (weak)
• Cytochrome P-450 CYP2C8 Inhibitors
• Cytochrome P-450 CYP2C8 Inhibitors (weak)
• Cytochrome P-450 CYP2C8 Substrates
• Cytochrome P-450 CYP2C9 Inhibitors
• Cytochrome P-450 CYP2C9 Inhibitors (weak)
• Cytochrome P-450 CYP2D6 Inhibitors
• Cytochrome P-450 CYP2D6 Inhibitors (weak)
• Cytochrome P-450 CYP3A Inhibitors
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Inhibitors
• Cytochrome P-450 CYP3A4 Inhibitors (weak)
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Dermatologicals
• Enzyme Inhibitors
• Fatty Acids
• Fatty Acids, Volatile
• Keratosis, Actinic, drug therapy
• Kinase Inhibitor
• Lipids
• MATE 1 Inhibitors
• MATE 2 Inhibitors
• MATE inhibitors
• Microtubule Inhibitors
• OATP1B1/SLCO1B1 Inhibitors
• OATP1B3 inhibitors
• OCT1 inhibitors
• OCT2 Inhibitors
• Oxazines
• Tubulin Inhibiting Agent
• Tyrosine Kinase Inhibitors

Classification

Not classified

Affected organisms

Not Available

Chemical Identifiers

UNII

4V9848RS5G

CAS number

897016-82-9

InChI Key

HUNGUWOZPQBXGX-UHFFFAOYSA-N

InChI

InChI=1S/C26H29N3O3/c30-26(28-19-21-4-2-1-3-5-21)18-24-9-6-23(20-27-24)22-7-10-25(11-8-22)32-17-14-29-12-15-31-16-13-29/h1-11,20H,12-19H2,(H,28,30)

IUPAC Name

N-benzyl-2-(5-{4-[2-(morpholin-4-yl)ethoxy]phenyl}pyridin-2-yl)acetamide

SMILES

O=C(CC1=CC=C(C=N1)C1=CC=C(OCCN2CCOCC2)C=C1)NCC1=CC=CC=C1

References

General References

1. Kempers S, DuBois J, Forman S, Poon A, Cutler E, Wang H, Cutler D, Fang J, Kwan R: Tirbanibulin Ointment 1% as a Novel Treatment for Actinic Keratosis: Phase 1 and 2 Results. J Drugs Dermatol. 2020 Nov 1;19(11):1093-1100. doi: 10.36849/JDD.2020.5576. [Article]
2. Niu L, Yang J, Yan W, Yu Y, Zheng Y, Ye H, Chen Q, Chen L: Reversible binding of the anticancer drug KXO1 (tirbanibulin) to the colchicine-binding site of beta-tubulin explains KXO1's low clinical toxicity. J Biol Chem. 2019 Nov 29;294(48):18099-18108. doi: 10.1074/jbc.RA119.010732. Epub 2019 Oct 18. [Article]
3. Cramer P, Stockfleth E: Actinic keratosis: where do we stand and where is the future going to take us? Expert Opin Emerg Drugs. 2020 Mar;25(1):49-58. doi: 10.1080/14728214.2020.1730810. Epub 2020 Feb 20. [Article]
4. Anbalagan M, Ali A, Jones RK, Marsden CG, Sheng M, Carrier L, Bu Y, Hangauer D, Rowan BG: Peptidomimetic Src/pretubulin inhibitor KX-01 alone and in combination with paclitaxel suppresses growth, metastasis in human ER/PR/HER2-negative tumor xenografts. Mol Cancer Ther. 2012 Sep;11(9):1936-47. doi: 10.1158/1535-7163.MCT-12-0146. Epub 2012 Jul 10. [Article]
5. Anbalagan M, Carrier L, Glodowski S, Hangauer D, Shan B, Rowan BG: KX-01, a novel Src kinase inhibitor directed toward the peptide substrate site, synergizes with tamoxifen in estrogen receptor alpha positive breast cancer. Breast Cancer Res Treat. 2012 Apr;132(2):391-409. doi: 10.1007/s10549-011-1513-3. Epub 2011 Apr 21. [Article]
6. Antonarakis ES, Heath EI, Posadas EM, Yu EY, Harrison MR, Bruce JY, Cho SY, Wilding GE, Fetterly GJ, Hangauer DG, Kwan MF, Dyster LM, Carducci MA: A phase 2 study of KX2-391, an oral inhibitor of Src kinase and tubulin polymerization, in men with bone-metastatic castration-resistant prostate cancer. Cancer Chemother Pharmacol. 2013 Apr;71(4):883-92. doi: 10.1007/s00280-013-2079-z. Epub 2013 Jan 13. [Article]
7. Dodds A, Chia A, Shumack S: Actinic keratosis: rationale and management. Dermatol Ther (Heidelb). 2014 Jun;4(1):11-31. doi: 10.1007/s13555-014-0049-y. Epub 2014 Mar 14. [Article]
8. Serrels B, Serrels A, Mason SM, Baldeschi C, Ashton GH, Canel M, Mackintosh LJ, Doyle B, Green TP, Frame MC, Sansom OJ, Brunton VG: A novel Src kinase inhibitor reduces tumour formation in a skin carcinogenesis model. Carcinogenesis. 2009 Feb;30(2):249-57. doi: 10.1093/carcin/bgn278. Epub 2008 Dec 5. [Article]
9. Kim S, Min A, Lee KH, Yang Y, Kim TY, Lim JM, Park SJ, Nam HJ, Kim JE, Song SH, Han SW, Oh DY, Kim JH, Kim TY, Hangauer D, Lau JY, Im K, Lee DS, Bang YJ, Im SA: Antitumor Effect of KX-01 through Inhibiting Src Family Kinases and Mitosis. Cancer Res Treat. 2017 Jul;49(3):643-655. doi: 10.4143/crt.2016.168. Epub 2016 Oct 6. [Article]
10. Anbalagan M, Sheng M, Fleischer B, Zhang Y, Gao Y, Hoang V, Matossian M, Burks HE, Burow ME, Collins-Burow BM, Hangauer D, Rowan BG: Dual Src Kinase/Pretubulin Inhibitor KX-01, Sensitizes ERalpha-negative Breast Cancers to Tamoxifen through ERalpha Reexpression. Mol Cancer Res. 2017 Nov;15(11):1491-1502. doi: 10.1158/1541-7786.MCR-16-0297-T. Epub 2017 Jul 27. [Article]
11. FDA Approved Drug Products: KLISYRI (tirbanibulin) ointment, for topical use [Link]
12. Drugs.com: Klisyri FDA Approval History [Link]
13. Cayman Chemical: KX2-391 Safety Data Sheet [Link]

External Links

ChemSpider

24633341

BindingDB

50303801

RxNav

2471078

ChEMBL

CHEMBL571546

ZINC

ZINC000043152787

PDBe Ligand

DN0

Wikipedia

Tirbanibulin

PDB Entries

6knz

Clinical Trials

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

Phase	Status	Purpose	Conditions	Count
4	Completed	Treatment	Actinic Keratosis (AK)	2
4	Not Yet Recruiting	Treatment	Actinic Keratosis (AK)	1
4	Recruiting	Treatment	Actinic Keratosis (AK)	1
3	Completed	Treatment	Actinic Keratosis (AK)	3
3	Not Yet Recruiting	Treatment	Actinic Keratosis (AK)	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Ointment	Cutaneous	10 mg/g
Ointment	Topical	10 mg/1g
Ointment	Topical	1 % w/w

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US7851470	No	2010-12-14	2029-02-02
US10617693	No	2020-04-14	2038-03-12
US8980890	No	2015-03-17	2025-12-28
US7300931	No	2007-11-27	2026-02-06
US10323001	No	2019-06-18	2027-12-28
US8236799	No	2012-08-07	2025-12-28
US10669236	No	2020-06-02	2038-09-07
US11497750	No	2018-03-12	2038-03-12

Properties

State

Solid

Experimental Properties

Not Available

Predicted Properties

Property	Value	Source
Water Solubility	0.0248 mg/mL	ALOGPS
logP	3.26	ALOGPS
logP	3.21	Chemaxon
logS	-4.2	ALOGPS
pKa (Strongest Acidic)	15.36	Chemaxon
pKa (Strongest Basic)	6.63	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	5	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	63.69 Å2	Chemaxon
Rotatable Bond Count	9	Chemaxon
Refractivity	124.86 m3·mol-1	Chemaxon
Polarizability	48.49 Å3	Chemaxon
Number of Rings	4	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	Yes	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Not Available

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0059-0319600000-7659c0d6da6d08ea0947
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0059-0269400000-d38d9b741932838fdc9b
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-01tc-1379000000-26b7ac1b5c35eb33a071
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-01t9-0397000000-113ccf59b5b3bea306dc
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-03yi-3921300000-63dfc6ae3ad5045660ea
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-008a-3962100000-c9f4f8a18a0bfde2b44f
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å2)	Source type	Source
[M-H]-	223.4084223	predicted	DarkChem Lite v0.1.0
[M+H]+	224.3539223	predicted	DarkChem Lite v0.1.0
[M+Na]+	223.4505223	predicted	DarkChem Lite v0.1.0

Targets

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Details1. Tubulin beta chain

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

Curator comments

Tirbanibulin binds to the colchicine-binding site of β-tubulin. Antonarakis et al. (2013) showed that IC50 for tubulin polymerization inhibition in human tumour cells is about 125 nM in the absence of plasma and about 500 nM in the presence of plasma. An approximate 4-fold reduction in potency for tubulin polymerization inhibition is attributed to extensive plasma protein binding of tirbanibulin (88%).

General Function

Ubiquitin protein ligase binding

Specific Function

Tubulin is the major constituent of microtubules. It binds two moles of GTP, one at an exchangeable site on the beta chain and one at a non-exchangeable site on the alpha chain.

Gene Name

TUBB

Uniprot ID

P07437

Uniprot Name

Tubulin beta chain

Molecular Weight

49670.515 Da

References

1. Niu L, Yang J, Yan W, Yu Y, Zheng Y, Ye H, Chen Q, Chen L: Reversible binding of the anticancer drug KXO1 (tirbanibulin) to the colchicine-binding site of beta-tubulin explains KXO1's low clinical toxicity. J Biol Chem. 2019 Nov 29;294(48):18099-18108. doi: 10.1074/jbc.RA119.010732. Epub 2019 Oct 18. [Article]
2. Anbalagan M, Ali A, Jones RK, Marsden CG, Sheng M, Carrier L, Bu Y, Hangauer D, Rowan BG: Peptidomimetic Src/pretubulin inhibitor KX-01 alone and in combination with paclitaxel suppresses growth, metastasis in human ER/PR/HER2-negative tumor xenografts. Mol Cancer Ther. 2012 Sep;11(9):1936-47. doi: 10.1158/1535-7163.MCT-12-0146. Epub 2012 Jul 10. [Article]

Details2. Proto-oncogene tyrosine-protein kinase Src

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

Curator comments

Tirbanibulin binds to the substrate-binding site of Src kinase. Antonarakis et al. (2013) showed that the IC50 for Src inhibition in human tumour cells is about 25 nM in the absence of human plasma and about 100 nM in the presence of human plasma. An approximate 4-fold reduction in potency for Src inhibition is attributed to extensive plasma protein binding of tirbanibulin (88%).

General Function

Sh3/sh2 adaptor activity

Specific Function

Non-receptor protein tyrosine kinase which is activated following engagement of many different classes of cellular receptors including immune response receptors, integrins and other adhesion recept...

Gene Name

SRC

Uniprot ID

P12931

Uniprot Name

Proto-oncogene tyrosine-protein kinase Src

Molecular Weight

59834.295 Da

References

1. Anbalagan M, Carrier L, Glodowski S, Hangauer D, Shan B, Rowan BG: KX-01, a novel Src kinase inhibitor directed toward the peptide substrate site, synergizes with tamoxifen in estrogen receptor alpha positive breast cancer. Breast Cancer Res Treat. 2012 Apr;132(2):391-409. doi: 10.1007/s10549-011-1513-3. Epub 2011 Apr 21. [Article]
2. Antonarakis ES, Heath EI, Posadas EM, Yu EY, Harrison MR, Bruce JY, Cho SY, Wilding GE, Fetterly GJ, Hangauer DG, Kwan MF, Dyster LM, Carducci MA: A phase 2 study of KX2-391, an oral inhibitor of Src kinase and tubulin polymerization, in men with bone-metastatic castration-resistant prostate cancer. Cancer Chemother Pharmacol. 2013 Apr;71(4):883-92. doi: 10.1007/s00280-013-2079-z. Epub 2013 Jan 13. [Article]

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Drug created at November 18, 2007 18:30 / Updated at February 21, 2021 18:51