WARNING: This product is for research use only, not for human or veterinary use.

MedKoo CAT#: 205494

CAS#: 1029712-80-8 (free base)

Description: Capmatinib, also known as INCB28060 and INC280, is an orally bioavailable inhibitor of the proto-oncogene c-Met (hepatocyte growth factor receptor [HGFR]) with potential antineoplastic activity. c-Met inhibitor INC280 selectively binds to c-Met, thereby inhibiting c-Met phosphorylation and disrupting c-Met signal transduction pathways. This may induce cell death in tumor cells overexpressing c-Met protein or expressing constitutively activated c-Met protein. Capmatinib was approved in 2020.

Chemical Structure

CAS# 1029712-80-8 (free base)

Theoretical Analysis

MedKoo Cat#: 205494
Name: Capmatinib
CAS#: 1029712-80-8 (free base)
Chemical Formula: C23H17FN6O
Exact Mass: 412.14
Molecular Weight: 412.420
Elemental Analysis: C, 66.98; H, 4.15; F, 4.61; N, 20.38; O, 3.88

Price and Availability

Size Price Availability Quantity
25mg USD 90 Ready to ship
50mg USD 150 Ready to ship
100mg USD 250 Ready to ship
200mg USD 450 Ready to ship
500mg USD 950 Ready to ship
1g USD 1650 Ready to ship
2g USD 2950 Ready to ship
5g USD 5850 Ready to ship
Bulk inquiry

Related CAS #: 1029712-80-8 (free base)   1865733-40-9 (HCl hydrate)   1029714-89-3 (xHCl)   1197376-85-4 (2HCl)   1197376-90-1 (besylate)   1450883-33-6 (fumarate)    

Synonym: INC280; INC-280; INC 280; INCB028060; INCB-028060; INCB 028060; INCB28060; INCB-28060; INCB 28060; Capmatinib.

IUPAC/Chemical Name: 2-fluoro-N-methyl-4-(7-(quinolin-6-ylmethyl)imidazo[1,2-b][1,2,4]triazin-2-yl)benzamide


InChi Code: InChI=1S/C23H17FN6O/c1-25-22(31)18-6-5-16(11-19(18)24)21-13-28-23-27-12-17(30(23)29-21)10-14-4-7-20-15(9-14)3-2-8-26-20/h2-9,11-13H,10H2,1H3,(H,25,31)


Appearance: Yellow solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO, not in water

Shelf Life: >2 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

More Info: INCB28060 exhibits picomolar enzymatic potency and is highly specific for c-MET with more than 10,000-fold selectivity over a large panel of human kinases. This inhibitor potently blocks c-MET phosphorylation and activation of its key downstream effectors in c-MET-dependent tumor cell lines. As a result, INCB28060 potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis in vitro. Oral dosing of INCB28060 results in time- and dose-dependent inhibition of c-MET phosphorylation and tumor growth in c-MET-driven mouse tumor models, and the inhibitor is well tolerated at doses that achieve complete tumor inhibition. In a further exploration of potential interactions between c-MET and other signaling pathways, we found that activated c-MET positively regulates the activity of epidermal growth factor receptors (EGFR) and HER-3, as well as expression of their ligands. These effects are reversed with INCB28060 treatment. Finally, we confirmed that circulating hepatocyte growth factor levels are significantly elevated in patients with various cancers. Activated c-MET has pleiotropic effects on multiple cancer-promoting signaling pathways and may play a critical role in driving tumor cell growth and survival. INCB28060 is a potent and selective c-MET kinase inhibitor that may have therapeutic potential in cancer treatment. (source: Clin Cancer Res; 17(22); 7127-38. ©2011 AACR.)       

Biological target: ATP competitive c-Met kinase inhibitor (IC50=0.13 nM)
In vitro activity: Pancreatic cancer is characterized by a strong stromal reaction. Therefore, the effects of cMET inhibition on ECs and VSMCs were examined. MTT assays in ECs under serum-starved conditions and stimulation with HGF, showed a slight but significant increase in growth that was diminished by INC280 (Capmatinib) (Additional file 3: Figure S3B). No effect upon constitutive conditions was observed (Additional file 3: Figure S3A). EC motility was significantly increased upon incubation with HGF, which was strongly reduced by INC280 (Figure 4A). Regarding activation of signaling pathways, treatment with INC280 strongly inhibited HGF-induced activation of Akt and ERK whereas no effects on constitutive Akt and ERK phosphorylation were found (Figure 4B). Taken together, these results show that INC280 affects ECs only when these cells are stimulated with HGF. Next we analyzed the impact of INC280 on VSMCs. MTT assays showed a dose-dependent inhibition of VSMC growth starting from INC280 (100nM) after 72 hours of incubation (Additional file 3: Figure S3C). In contrast to ECs, stimulation with HGF upon serum-starved conditions had no effect on VSMC growth and, accordingly, INC280 did not have a further growth inhibitory effect in MTT assays (Additional file 3: Figure S3D). Motility upon incubation with HGF in VSMCs was not induced, but targeting cMET with INC280 led to a significant inhibition of constitutive migration (Figure 4C). Finally, Western blotting did not show a substantial effect of INC280 on constitutive Akt phosphorylation and only a minor impact on ERK phosphorylation in VSMCs (Figure 4D). These results indicate that HGF does not affect VSMCs and cMET inhibition with INC280, therefore, has only minor effects on these cells. Reference: BMC Cancer. 2015; 15: 71.
In vivo activity: Tumors underwent a histological examination by a pathologist to determine phenotype and progression. Of the WT mice fed normal diet there were a total of 16 tumors. Twelve of the tumors were papillomas, with one converting to a squamous cell carcinoma (Fig.4d). Three additional tumors were cutaneous lipomas. This is in comparison to Tpl2 −/− mice which had a total of 61 tumors, 51 papillomas, four SCCs, three sebaceous adenomas, and three lipomas. In contrast, no Tpl2 −/− mice fed capmatinib diet had papillomas convert to SCCs (Fig. (Fig.4d).4d). Although Tpl2 −/− mice develop an overall higher tumor burder, there were no statistical differences in tumor size between genotypes and the rate of malignant conversion (7.8 vs. 8.3%) was similar between Tpl2 −/− and WT mice on normal diet. However, the rate of malignant conversion between Tpl2 −/− mice on normal diet (8.3%) vs. Tpl2 −/− mice on Capmatinib diet (0%) was significantly different (p < 0.01). In both genotypes male mice developed more tumors than female mice (Fig.4e; p < 0.05). Reference: Oncogenesis. 2019 Jan; 8(1): 1.

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
DMF 1.0 2.42
DMF:PBS (pH 7.2) (1:3) 0.3 0.61
DMSO 9.1 22.06
Water 10.0 24.25

Preparing Stock Solutions

The following data is based on the product molecular weight 412.42 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
Formulation protocol: 1. Brandes F, Schmidt K, Wagner C, Redekopf J, Schlitt HJ, Geissler EK, Lang SA. Targeting cMET with INC280 impairs tumour growth and improves efficacy of gemcitabine in a pancreatic cancer model. BMC Cancer. 2015 Feb 19;15:71. doi: 10.1186/s12885-015-1064-9. PMID: 25884642; PMCID: PMC4340491. 2. Bonan NF, Kowalski D, Kudlac K, Flaherty K, Gwilliam JC, Falkenberg LG, Maradiaga E, DeCicco-Skinner KL. Inhibition of HGF/MET signaling decreases overall tumor burden and blocks malignant conversion in Tpl2-related skin cancer. Oncogenesis. 2019 Jan 10;8(1):1. doi: 10.1038/s41389-018-0109-8. PMID: 30631034; PMCID: PMC6328619.
In vitro protocol: 1. Brandes F, Schmidt K, Wagner C, Redekopf J, Schlitt HJ, Geissler EK, Lang SA. Targeting cMET with INC280 impairs tumour growth and improves efficacy of gemcitabine in a pancreatic cancer model. BMC Cancer. 2015 Feb 19;15:71. doi: 10.1186/s12885-015-1064-9. PMID: 25884642; PMCID: PMC4340491.
In vivo protocol: 1. Bonan NF, Kowalski D, Kudlac K, Flaherty K, Gwilliam JC, Falkenberg LG, Maradiaga E, DeCicco-Skinner KL. Inhibition of HGF/MET signaling decreases overall tumor burden and blocks malignant conversion in Tpl2-related skin cancer. Oncogenesis. 2019 Jan 10;8(1):1. doi: 10.1038/s41389-018-0109-8. PMID: 30631034; PMCID: PMC6328619.

Molarity Calculator

Calculate the mass, volume, or concentration required for a solution.

*When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and SDS / CoA (available online).

Reconstitution Calculator

The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.


Dilution Calculator

Calculate the dilution required to prepare a stock solution.

1: Paik PK, Goyal RK, Cai B, Price MA, Davis KL, Ansquer VD, Caro N, Saliba TR. Real-world outcomes in non-small-cell lung cancer patients with MET Exon 14 skipping mutation and brain metastases treated with capmatinib. Future Oncol. 2023 Feb 7. doi: 10.2217/fon-2022-1133. Epub ahead of print. PMID: 36749292.

2: Yang M, Vioix H, Sachdev R, Stargardter M, Tosh J, Pfeiffer BM, Paik PK. Cost-Effectiveness of Tepotinib versus Capmatinib for the Treatment of Adult Patients with Metastatic Non-Small Cell Lung Cancer Harboring Mesenchymal- epithelial Transition Exon 14 (METex14) Skipping. Value Health. 2022 Dec 8:S1098-3015(22)04750-7. doi: 10.1016/j.jval.2022.11.018. Epub ahead of print. PMID: 36503033.

3: Zayed A, Jaber SA, Al Hroot J, Hawamdeh S, Ayoub NM, Qinna NA. HPLC with Fluorescence and Photodiode Array Detection for Quantifying Capmatinib in Biological Samples: Application to In Vivo and In Vitro Studies. Molecules. 2022 Dec 5;27(23):8582. doi: 10.3390/molecules27238582. PMID: 36500674; PMCID: PMC9738601.

4: Turpin A, Descarpentries C, Grégoire V, Farchi O, Cortot AB, Jamme P. Response to Capmatinib in a MET Fusion-positive Cholangiocarcinoma. Oncologist. 2023 Jan 18;28(1):80-83. doi: 10.1093/oncolo/oyac194. PMID: 36434677; PMCID: PMC9847551.

5: Choi W, Jeong KC, Park SY, Kim S, Kang EH, Hwang M, Han JY. MYC amplification-conferred primary resistance to capmatinib in a MET-amplified NSCLC patient: a case report. Transl Lung Cancer Res. 2022 Sep;11(9):1967-1972. doi: 10.21037/tlcr-22-176. PMID: 36248327; PMCID: PMC9554684.

6: Tseng LW, Chang JW, Wu CE. Safety of Tepotinib Challenge after Capmatinib- Induced Pneumonitis in a Patient with Non-Small Cell Lung Cancer Harboring MET Exon 14 Skipping Mutation: A Case Report. Int J Mol Sci. 2022 Oct 5;23(19):11809. doi: 10.3390/ijms231911809. PMID: 36233109; PMCID: PMC9570266.

7: Bhangare D, Rajput N, Jadav T, Sahu AK, Sengupta P. Mechanism of capmatinib degradation in stress conditions including degradation product characterization using ultra-high-performance liquid chromatography-quadrupole-time of flight mass spectrometry and stability-indicating analytical method development. Rapid Commun Mass Spectrom. 2023 Jan 15;37(1):e9417. doi: 10.1002/rcm.9417. PMID: 36226771.

8: Wilgucki M, Yeung V, Ho G, Bravo Montenegro GL, Jones G, Reuss JE, Liu SV, Kim C. Osimertinib and Capmatinib Combination Therapy to Overcome MET Y1003N-Mediated Resistance in EGFR-Mutant NSCLC: A Case Report. JTO Clin Res Rep. 2022 Aug 5;3(10):100396. doi: 10.1016/j.jtocrr.2022.100396. PMID: 36188633; PMCID: PMC9516460.

9: Chen X, Isambert N, López-López R, Giovannini M, Pognan N, Kapoor S, Quinlan M, You B, Cui X, Rahmanzadeh G, Mau-Sorensen M. Effect of capmatinib on the pharmacokinetics of substrates of CYP3A (midazolam) and CYP1A2 (caffeine) in patients with MET-dysregulated solid tumours. Br J Clin Pharmacol. 2023 Mar;89(3):1046-1055. doi: 10.1111/bcp.15544. Epub 2022 Oct 17. PMID: 36131603.

10: Cui X, Chen X, Pognan N, Sengupta T, Rahmanzadeh G, Kornberger R, Giovannini M. Evaluation of the Pharmacokinetic Drug Interaction of Capmatinib With Itraconazole and Rifampicin and Potential Impact on Renal Transporters in Healthy Subjects. J Clin Pharmacol. 2023 Feb;63(2):228-238. doi: 10.1002/jcph.2153. Epub 2022 Nov 2. PMID: 36087217.

11: Kim TW, Lee KM, Lee SH. Capmatinib in MET Exon 14 Skipping Mutation-Positive Lung Adenocarcinoma with Extensive Central Nervous System Metastasis. Onco Targets Ther. 2022 Aug 31;15:941-946. doi: 10.2147/OTT.S382722. PMID: 36072511; PMCID: PMC9441579.

12: Lin CY, Wei SH, Chen YL, Lee CT, Wu SY, Ho CL, Pavlick DC, Su PL, Lin CC. Case report: Salvage capmatinib therapy in KIF5B-MET fusion-positive lung adenocarcinoma with resistance to telisotuzumab vedotin. Front Oncol. 2022 Aug 11;12:919123. doi: 10.3389/fonc.2022.919123. PMID: 36033470; PMCID: PMC9404301.

13: Illini O, Fabikan H, Swalduz A, Vikström A, Krenbek D, Schumacher M, Dudnik E, Studnicka M, Öhman R, Wurm R, Wannesson L, Peled N, Kian W, Bar J, Daher S, Addeo A, Rotem O, Pall G, Zer A, Saad A, Cufer T, Sorotsky HG, Hashemi SMS, Mohorcic K, Stoff R, Rovitsky Y, Keren-Rosenberg S, Winder T, Weinlinger C, Valipour A, Hochmair MJ. Real-world experience with capmatinib in MET exon 14-mutated non-small cell lung cancer (RECAP): a retrospective analysis from an early access program. Ther Adv Med Oncol. 2022 Jun 13;14:17588359221103206. doi: 10.1177/17588359221103206. PMID: 35720834; PMCID: PMC9201318.

14: Fujino T, Suda K, Koga T, Hamada A, Ohara S, Chiba M, Shimoji M, Takemoto T, Soh J, Mitsudomi T. Foretinib can overcome common on-target resistance mutations after capmatinib/tepotinib treatment in NSCLCs with MET exon 14 skipping mutation. J Hematol Oncol. 2022 Jun 11;15(1):79. doi: 10.1186/s13045-022-01299-z. PMID: 35690785; PMCID: PMC9188708.

15: Brazel D, Zhang S, Nagasaka M. Spotlight on Tepotinib and Capmatinib for Non-Small Cell Lung Cancer with MET Exon 14 Skipping Mutation. Lung Cancer (Auckl). 2022 May 13;13:33-45. doi: 10.2147/LCTT.S360574. PMID: 35592355; PMCID: PMC9113513.

16: Park HS, Abd El-Aty AM, Jeong JH, Lee T, Jung TW. Capmatinib suppresses LPS- induced interaction between HUVECs and THP-1 monocytes through suppression of inflammatory responses. Biomed J. 2022 Apr 26:S2319-4170(22)00071-3. doi: 10.1016/ Epub ahead of print. PMID: 35483573.

17: Chou YT, Lin CC, Lee CT, Pavlick DC, Su PL. Durable Response of Dabrafenib, Trametinib, and Capmatinib in an NSCLC Patient With Co-Existing BRAF-KIAA1549 Fusion and MET Amplification: A Case Report. Front Oncol. 2022 Mar 18;12:838798. doi: 10.3389/fonc.2022.838798. PMID: 35372088; PMCID: PMC8972191.

18: Hashiguchi MH, Sato T, Yamamoto H, Watanabe R, Kagyo J, Domoto H, Shiomi T. Successful Tepotinib Challenge After Capmatinib-Induced Interstitial Lung Disease in a Patient With Lung Adenocarcinoma Harboring MET Exon 14 Skipping Mutation: Case Report. JTO Clin Res Rep. 2021 Dec 28;3(2):100271. doi: 10.1016/j.jtocrr.2021.100271. PMID: 35252894; PMCID: PMC8888201.

19: Lefler DS, Tierno MB, Bashir B. Partial treatment response to capmatinib in MET-amplified metastatic intrahepatic cholangiocarcinoma: case report & review of literature. Cancer Biol Ther. 2022 Dec 31;23(1):112-116. doi: 10.1080/15384047.2022.2029128. PMID: 35129063; PMCID: PMC8820818.

20: Guo MZ, Marrone KA, Spira A, Waterhouse DM, Scott SC. Targeted Treatment of Non-Small Cell Lung Cancer: Focus on Capmatinib with Companion Diagnostics. Onco Targets Ther. 2021 Nov 23;14:5321-5331. doi: 10.2147/OTT.S273357. PMID: 34853516; PMCID: PMC8627896.