| Identification | Back Directory | [Name]
Glumetinib | [CAS]
1642581-63-2 | [Synonyms]
SCC244
Glumetinib
GLUMETINIB (SCC244)
1H-Pyrazolo[4,3-b]pyridine, 6-(1-methyl-1H-pyrazol-4-yl)-1-[[6-(1-methyl-1H-pyrazol-4-yl)imidazo[1,2-a]pyridin-3-yl]sulfonyl]- | [Molecular Formula]
C21H17N9O2S | [MDL Number]
MFCD31693844 | [MOL File]
1642581-63-2.mol | [Molecular Weight]
459.48 |
| Chemical Properties | Back Directory | [density ]
1.61±0.1 g/cm3(Predicted) | [storage temp. ]
-20°C | [solubility ]
Soluble in DMSO (>25 mg/ml) | [form ]
solid | [pka]
0.09±0.10(Predicted) | [color ]
Beige | [Stability:]
Stable for 1 year as supplied. Solutions in DMSO may be stored at -20°C for up to 1 month. |
| Hazard Information | Back Directory | [Description]
Glumetinib (1642581-63-2) is a highly selective (2400-fold selectivity against a panel of 312 kinases) and potent (IC50 = 0.42 nM) inhibitor of c-Met kinase.? It induced tumor regression in MET-driven CDX (MKN-45, SNU-5, EBC-1) and PDX (4 NSCLC, 5 HCC) tumor models. | [Uses]
Glumetinib (SCC244) is a highly selective, orally bioavailable, ATP-competitive c-Met inhibitor with an IC50 of 0.42 nM. Glumetinib has greater than 2400-fold selectivity for c-Met over those 312 kinases evaluated, including the c-Met family member RON and highly homologous kinases Axl, Mer, TyrO3. Antitumor activity[1]. | [in vivo]
Glumetinib (2.5-10 mg/kg; p.o.; once daily for 2-3 weeks) significantly inhibits c-Met–driven tumor growth in cancer CDX models[1].
Glumetinib shows significant antitumor efficiency in NSCLC and HCC tumor PDX models with MET aberration[1]. | Animal Model: | Female nude mice (4-6 weeks old) (MKN-45 model)[1] | | Dosage: | 10, 5, 2.5 mg/kg | | Administration: | P.o.; once daily for 2-3 weeks | | Result: | Significantly inhibited tumor growth with inhibitory rates of 99.3%, 88.6%, and 63.6% at doses of 10, 5, and 2.5 mg/kg, respectively.
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| [References]
Ai et al. (2018), Preclinical Evaluation of SCC244 (Glumetinib), a Novel, Potent, and Highly Selective Inhibitor of c-Met in MET-dependent Cancer Models; Cancer Res., 17 751 |
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