ChemicalBook CAS DataBase List 2642037-07-6

2642037-07-6

Name	RMC-4998
CAS	2642037-07-6
Molecular Formula	C57H74N8O7
Molecular Weight	983.25
MOL File	2642037-07-6.mol

Chemical Properties

density	1.24±0.1 g/cm3(Temp: 20 °C; Press: 760 Torr)(Predicted)
form	Solid
pka	13.44±0.40(Predicted)
color	White to off-white

Hazard Information

Uses

RMC-4998 is an orally active inhibitor targeting the active or GTP-bound state of the KRASG12C mutant. RMC-4998 can form a ternary complex with intracellular CYPA and the activated KRASG12C mutant, with an IC50 value of 28 nM. RMC-4998 can inhibit ERK signaling in KRASG12C mutant cancer cells and induce apoptosis. RMC-4998 can be used for tumor research[1][2].

in vivo

RMC-4998 (10-200 mg/kg; once daily; 28 days; p.o.) inhibits ERK phosphorylation in tumors and exhibits anti-tumor activity in mice carrying NCI-H358 xenografts^[1]. RMC-4998 (80 mg/kg; once daily; 4 weeks; p.o.) can promote tumor regression in non-small cell lung cancer mice and has anti-tumor activity^[2]. RMC-4998 (100 mg/kg; once daily; p.o.) induces tumor regression and inhibits ERK phosphorylation expression in sotorasib-R LU65 xenograft mice^[3].

Animal Model:	Mice model bearing H358 CDX tumors^[1].
Dosage:	10-200 mg/kg
Administration:	Oral gavage (p.o.); once daily; 28 days
Result:	Inhibited ERK phosphorylation in tumors for about 24 hours and induced cell apoptosis, leading to tumor regression.

Animal Model:	The cell-line derived H2122 KRASG12C lung adenocarcinoma xenograft model (CDX)^[2].
Dosage:	80 mg/kg
Administration:	Oral gavage (p.o.); once daily; 4 weeks
Result:	Inhibited tumor growth for 30-35 days.

Animal Model:	Sotorasib-R LU65 mice xenograft model^[3].
Dosage:	100 mg/kg
Administration:	Oral gavage (p.o.); once dailys
Result:	Reduced tumor volume and lowered the expression of pERK protein in the tumor.

References

[1] Schulze CJ, et al. Chemical remodeling of a cellular chaperone to target the active state of mutant KRAS. Science. 2023 Aug 18;381(6659):794-799. DOI:10.1126/science.adg9652
[2] Kitai H,et al. Combined inhibition of KRASG12C and mTORC1 kinase is synergistic in non-small cell lung cancer. Nat Commun. 2024 Jul 19;15(1):6076. DOI:10.1038/s41467-024-50063-z
[3] Solanki H S, et al. RTK signaling and WT RAS activity as vulnerabilities in tumors with acquired resistance to GDP-state selective KRASG12C inhibitors in preclinical models[J]. Cancer Research, 2024, 84(6_Supplement): 1924-1924.

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