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RMC-7977

Catalog No. T81263 CAS 2765082-12-8

RMC-7977 is a reversible triple complex RAS inhibitor that exhibits broad-spectrum activity against mutant and wild-type (WT) variants of KRAS, NRAS, and HRAS. The compound is capable of triggering tumor regression and has shown good tolerability in a variety of RAS-dependent preclinical cancer models. In addition, RMC-7977 effectively inhibited the growth of KRASG12C cancer tumor models.[1]

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RMC-7977, CAS 2765082-12-8

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1 mg	In stock	$ 1,930.00
5 mg	In stock	$ 4,086.00
10 mg	In stock	Inquiry

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Purity: 97.46%

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Description	RMC-7977 is a reversible triple complex RAS inhibitor that exhibits broad-spectrum activity against mutant and wild-type (WT) variants of KRAS, NRAS, and HRAS. The compound is capable of triggering tumor regression and has shown good tolerability in a variety of RAS-dependent preclinical cancer models. In addition, RMC-7977 effectively inhibited the growth of KRASG12C cancer tumor models.[1]
In vitro	METHODS: U2OS cells were treated with 50 nM RMC-7977 to observe the formation of KRAS-CYPA complexes and disruption of KRAS(G12V)-CRAF interactions using a live-cell nano-bioluminescence resonance energy transfer (BRET) kinetic assay. RESULTS: RMC-7977 induced KRAS and CYPA binding and dissociated the CRAF RBD from KRAS at the same fast rate (signaling half-life (t1/2) < 5 min).[1] METHODS: RAS-dependent (KRAS, NRAS, or EGFR mutated) cancer cells treated with RMC-7977 (0.1,1,10,100,100 nM) were compared for activity of RMC-7977 in cancer cells harboring various activating mutations in the RAS pathway, specifically oncogenic variants of KRAS, NRAS, EGFR, or BRAF. RESULTS: Exhibited concentration-dependent inhibition of downstream signaling and proliferation in the low nanomolar range.[1]
In vivo	METHODS: U2OS cells were treated with 50 nM RMC-7977 to observe the formation of KRAS-CYPA complexes and disruption of KRAS(G12V)-CRAF interactions using a live-cell nano-bioluminescence resonance energy transfer (BRET) kinetic assay. RESULTS: RMC-7977 induced KRAS and CYPA binding and dissociated the CRAF RBD from KRAS at the same fast rate (signaling half-life (t1/2) < 5 min).[1] METHODS: RAS-dependent (KRAS, NRAS, or EGFR mutated) cancer cells treated with RMC-7977 (0.1,1,10,100,100 nM) were compared for activity of RMC-7977 in cancer cells harboring various activating mutations in the RAS pathway, specifically oncogenic variants of KRAS, NRAS, EGFR, or BRAF. RESULTS: Exhibited concentration-dependent inhibition of downstream signaling and proliferation in the low nanomolar range.[1]

Molecular Weight	865.09
Formula	C47H60N8O6S
CAS No.	2765082-12-8

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store at low temperature,keep away from direct sunlight

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

References and Literature

1. Holderfield M,et al. Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy. Nature. 2024 Apr 8. 2. Wasko UN, et al. Tumor-selective effects of active RAS inhibition in pancreatic ductal adenocarcinoma. bioRxiv [Preprint]. 2023 Dec 4:2023.12.03.569791.

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Keywords

RMC-7977 2765082-12-8 GPCR/G Protein MAPK Ras inhibitor inhibit

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