Tepotinib | Selective c-MET inhibitor
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $60.00 | ||
| 25 mg | $200.00 |
Tepotinib (1100598-32-0) is a selective type 1b MET inhibitor. In biochemical assays using His6-tagged recombinant human MET kinase domain, tepotinib inhibited kinase activity in a concentration-dependent manner with IC50=1.8 nM.1 It displays marked antitumor activity in MET-dependent tumor models.2 It crosses the blood-brain barrier and displays intracranial antitumor activity.3 Tepotinib can overcome EGFR inhibitor resistance mediated by aberrant c-Met activation4 and is in clinical use for non-small cell lung cancer harboring MET exon 14 skipping alterations.
References/Citations:
- Albers et al. (2023), The Preclinical Pharmacology of Tepotinib – A Highly Selective MET Inhibitor with Activity in Tumors Harboring MET Alterations; Mol. Cancer Ther. 22 833
- Bladt et al. (2013), EMD 1214063 and EMD 1204831 constitute a new class of potent and highly selective c-MET inhibitors; Clin. Cancer Res. 19 2941
- Friese-Hamim et al. (2022), Brain penetration and efficacy of tepotinib in orthotopic patient-derived xenograft models of MET-driven non-small cell lung cancer in brain metastases; Lung Cancer 163 77
- Friese-Hamim et al. (2017), The selective c-MET inhibitor tepotinib can overcome epidermal growth factor receptor inhibitor resistance mediated by aberrant c-MET activation in NSCLC models; Am. J. Cancer Res. 7 962
C29H28N6O2
>98% TLC
NMR: (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
Tepotinib (1100598-32-0) is a selective type 1b MET inhibitor. In biochemical assays using His6-tagged recombinant human MET kinase domain, tepotinib inhibited kinase activity in a concentration-dependent manner with IC50=1.8 nM.1 It displays marked antitumor activity in MET-dependent tumor models.2 It crosses the blood-brain barrier and displays intracranial antitumor activity.3 Tepotinib can overcome EGFR inhibitor resistance mediated by aberrant c-Met activation4 and is in clinical use for non-small cell lung cancer harboring MET exon 14 skipping alterations.
References/Citations:
- Albers et al. (2023), The Preclinical Pharmacology of Tepotinib – A Highly Selective MET Inhibitor with Activity in Tumors Harboring MET Alterations; Mol. Cancer Ther. 22 833
- Bladt et al. (2013), EMD 1214063 and EMD 1204831 constitute a new class of potent and highly selective c-MET inhibitors; Clin. Cancer Res. 19 2941
- Friese-Hamim et al. (2022), Brain penetration and efficacy of tepotinib in orthotopic patient-derived xenograft models of MET-driven non-small cell lung cancer in brain metastases; Lung Cancer 163 77
- Friese-Hamim et al. (2017), The selective c-MET inhibitor tepotinib can overcome epidermal growth factor receptor inhibitor resistance mediated by aberrant c-MET activation in NSCLC models; Am. J. Cancer Res. 7 962
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Focus Biomolecules • Plymouth Meeting, PA USA • 1-855-FOCUS21
Focus Biomolecules
Plymouth Meeting, PA USA
1-855-FOCUS21
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