kras g12c

KRAS G12C inhibitor 16 is a potent inhibitor of KRAS G12C.

KRas G12C inhibitor 1 is a compound that selectively inhibits the KRas G12C protein.

KRAS G12C Inhibitor 13 is a specific inhibitor targeting the KRAS G12C mutation.

KRAS G12C inhibitor 14 is a potent compound with an IC₅₀ of 18 nM [1].

KRAS G12C inhibitor 15 is a potent inhibitor of the KRAS G12C protein.

KRAS G12C inhibitor 17 is a potent inhibitor of the KRAS G12C protein.

KRas G12C inhibitor 2 is a compound specifically designed to inhibit the KRas G12C mutation.

KRas G12C inhibitor 3 is a compound that specifically inhibits the KRas G12C mutation.

KRas G12C inhibitor 4 is a compound that inhibits KRas G12C.

KRAS G12C inhibitor 5 is a KRas G12C inhibitor. (Add a sentence that describes its primary function, mechanism, or application.)

KRAS G12C inhibitor 19 is a potent KRAS G12C inhibitor that demonstrates anti-tumor activity in cellular assays and inhibits tumor growth [1].

BI-2865 is a non-covalent pan-KRAS inhibitor.BI-2865 binds to KRAS WT, G12C, G12D, G12V, and G13D mutants with KD values of 6.9, 4.5, 32, 26, and 4.3 nM, respectively.BI-2865 showed antiproliferative activity in BaF3 cells expressing KRAS G12C, G12D, or G12V mutants[1] . BI-2865 showed antiproliferative activity on BaF3 cells expressing KRAS G12C, G12D or G12V mutants, with an average IC₅₀ value of approximately 140 nM.[1]

Adagrasib (MRTX849) is an orally active and selective covalent inhibitor of KRAS G12C. Adagrasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Adagrasib exhibits inhibitory activity against KRAS G12C mutant tumors.

Sotorasib (AMG-510) is an orally active and selective covalent inhibitor of KRAS G12C. Sotorasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Sotorasib exhibits inhibitory activity against KRAS G12C mutant tumors.

Divarasib (GDC-6036) is an investigational, oral, high-potency and selective KRAS G12C inhibitor with an IC₅₀ of <0.01 μM. Divarasib irreversibly locks KRAS G12C oncoprotein in an inactive state and inhibits tumor cell growth. It is being investigated for use in solid tumors, including non-small cell lung and colorectal cancers and other types of cancer.

BI-2852 is a KRAS inhibitor targeting the switch I/II pocket (SI/II-pocket) with nanomolar affinity, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.

RMC-6291 is an orally active, covalent inhibitor of KRAS G12C (ON) that forms a tri-complex within tumor cells between KRAS G12C (ON) and cyclophilin A (CypA), thereby preventing KRAS G12C (ON) from signaling via steric blockade of RAS effector binding and eliciting deep and durable suppression of RAS pathway activity in KRAS G12C tumor models [1].

ARS-1323 is the racemate of ARS-1620 and a mutant K-ras G12C inhibitor.

ARS-1630 is a mutant K-ras G12C inhibitor. It is a less active enantiomer of ARS-1620.

1588-A4 (ARS-1620 Intermediate) is an intermediate of ARS-1620 which is an atropisomeric selective KRASG12C inhibitor with desirable pharmacokinetics.

ARS-1323-alkyne is a switch-II pocket (S-IIP) inhibitor and a conformational specific chemical reporter of KRASG12C nucleotide state in living cells.

K-Ras G12C-IN-2 is a covalent KRAS G12C inhibitor.

K-Ras G12C-IN-4, is a potent Covalent Inhibitor of KRASG12C..

KRAS inhibitor-6 is a potent inhibitor of the KRAS G12C variant.