RMC-4998 (TFA)

RMC-4998 TFA is an orally active inhibitor targeting the active or GTP-bound state of the KRASG12C mutant. RMC-4998 TFA can form a ternary complex with intracellular CYPA and the activated KRASG12C mutant, with an IC50 value of 28 nM. RMC-4998 TFA can inhibit ERK signaling in KRASG12C mutant cancer cells and induce apoptosis. RMC-4998 TFA can be used for for non-small cell lung cancer (NSCLC) research[1][2][3].

Product Specifications

UNSPSC

12352005

Target

Apoptosis; ERK; mTOR; PI3K; Ras

Related Pathways

Apoptosis; GPCR/G Protein; MAPK/ERK Pathway; PI3K/Akt/mTOR; Stem Cell/Wnt

Field of Research

Cancer

Purity

99.02

Smiles

O=C(N1CCC[C@@H](C2=O)N1)[C@@H](NC([C@H](C(C)C)N3C([C@@]4(CCN(C(C#CC(C)(C)N(C)C)=O)C4)CC3)=O)=O)CC5=CC(C6=CC(C(CC(C)(C)CO2)=[C@@]([C@@]7=C([C@H](C)OC)N=CC=C7)N8CC)=C8C=C6)=CC=C5.FC(F)(F)C(O)=O

Molecular Formula

C59H75F3N8O9

Molecular Weight

1097.27

References & Citations

[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.|[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.|[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.