K-Ras Inhibitor

K-Ras Inhibitors (167):

Cat. No.	Product Name	Effect	Purity

HY-114277

Sotorasib	Inhibitor	99.75%
Sotorasib (AMG-510) is a first-in-class, orally bioavailable, and selective KRAS G12C covalent inhibitor. Sotorasib irreversibly inhibits KRAS G12C by locking it in an inactive GDP-bound state. Sotorasib leads to the regression of KRAS G12C‑mutated locally advanced or metastatic non‑small cell lung cancer (NSCLC).

HY-134813

MRTX1133	Inhibitor	99.97%
MRTX1133 is a noncovalent, potent, and selective alkyne-based KRAS G12D inhibitor. MRTX1133 optimally fills the switch II pocket and extends three substituents to favorably interact with the protein, resulting in an estimated K_D against KRAS G12D of 0.2 pM. MRTX1133 prevents SOS1-catalyzed nucleotide exchange and/or formation of the KRAS G12D/GTP/RAF1 complex, thereby inhibiting mutant KRAS-dependent signal transduction. MRTX1133 selectively inhibits KRAS G12D mutant, but not KRAS wild-type, tumor cells. MRTX1133 has single digit nanomolar activity in cellular assays and marked in vivo efficacy in tumor models harboring KRAS G12D mutations.

HY-148439

Daraxonrasib	Inhibitor	99.88%
Daraxonrasib (RMC-6236) is an orally active, non-covalent RAS (ON) inhibitor. Daraxonrasib disrupts the interaction of wild-type or mutant RAS proteins with the RAS binding domain of BRAF, with EC₅₀ values ranging from 28-220 nM for wild-type KRAS, NRAS, HRAS, and multiple oncogenic RAS variants. Daraxonrasib inhibits pERK. Daraxonrasib has anti-tumor activity against KRAS mutant tumors.

HY-130149

Adagrasib	Inhibitor	99.79%
Adagrasib (MRTX849) is a potent, orally-available, and mutation-selective covalent inhibitor of KRAS G12C with potential antineoplastic activity. Adagrasib covalently binds to KRAS G12C at the cysteine at residue 12, locks the protein in its inactive GDP-bound conformation, and inhibits KRAS-dependent signal transduction.

HY-156498

RMC-7977	Inhibitor	99.48%
RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (K_d = 195 nM) and KRAS (G12V) (K_d = 292 μM). It exhibits broad-spectrum inhibitory activity against KRAS, NRAS, and HRAS proteins and their various wild-type and mutant variants. RMC-7977 induces apoptosis by inhibiting the phosphorylation of ERK, CRAF, and RSK, as well as increasing PARP cleavage. This leads to tumor regression, reduces resistance in KRAS^G12C cancer models, and demonstrates good tolerability across various RAS cancer models.

HY-173637

AZD0022	Inhibitor	98.36%
AZD0022 is a selective and orally active KRAS^G12D inhibitor. AZD0022 inhibits KRAS pathway suppression in the GP2D xenograft model.

HY-176523

KRAS G12D-IN-29	Inhibitor
KRAS G12D inhibitor 29 (Compound Formula (I)) is an orally active and selective KRAS^G12D mutant inhibitor. KRAS G12D inhibitor 29 blocks downstream signaling pathways mediated by KRAS^G12D, suppressing tumor cell proliferation. KRAS G12D inhibitor 29 is promising for research of KRAS^G12D mutation-related cancers (such as pancreatic cancer, lung cancer, colorectal cancer).

HY-176785S

MCB-294	Inhibitor
MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with K_ds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC₅₀s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS^G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer.

HY-156819

Zoldonrasib	Inhibitor	99.73%
Zoldonrasib (RMC-9805) is a potent and orally active KRAS G12D inhibitor.Zoldonrasib induces apoptosis in KRAS G12D mutant cancer cells. Zoldonrasib has the potential for the research of KRAS G12D mutant cancer.

HY-145928

Divarasib	Inhibitor	99.31%
Divarasib (GDC-6036) is an orally bioavailable, highly potent, and selective KRAS G12C inhibitor with an IC₅₀ of <0.01 μM. Divarasib covalently binds to the switch II (SW-II) pocket of KRAS G12C and irreversibly locks it in the inactive GDP-bound state.

HY-125817

BI-3406	Inhibitor	99.95%
BI-3406 (compound I-6) is an orally active, highly potent and selective inhibitor of the interaction between KRAS and Son of Sevenless 1 (SOS1) with an IC₅₀ of 6 nM. BI-3406 potently reduces the formation of GTP-loaded KRAS, and inhibits MAPK pathway signaling. BI-3406 has anticancer activity.

HY-153346

Elironrasib	Inhibitor	99.65%
Elironrasib is an orally active and covalent inhibitor of KRAS^G12C(ON). Elironrasib forms a tri-complex within tumor cells between KRAS^G12C(ON) and cyclophilin A (CypA). Thus, Elironrasib prevents KRAS^G12C(ON) from signaling via steric blockade of RAS effector binding. Elironrasib inhibits ERK signaling and induced apoptosis in KRASG12C-mutant H358 cells. Elironrasib also inhibits the proliferation of KRAS^G12C mutant cells with a median IC₅₀ of 0.11 nM.

HY-126247

BI-2852	Inhibitor	99.57%
BI-2852 is a KRAS inhibitor for the switch I/II pocket (SI/II-pocket) by structure-based agent design with nanomolar affinity. BI-2852 is mechanistically distinct from covalent KRASG12C inhibitor (binds to switch II pocket) and binds ten-fold more strongly to active KRASG12D versus KRASwt (740 nM vs 7.5 μM). BI-2852 blocks GEF, GAP, and effector interactions with KRAS, leading to inhibition of downstream signaling and an antiproliferative effect in KRAS mutant cells.

HY-137516

LC-2	Inhibitor	98.48%
LC-2 is a potent and first-in-class von Hippel-Lindau-based PROTAC capable of degrading endogenous KRAS G12C, with DC₅₀s between 0.25 and 0.76 μM. LC-2 covalently binds KRAS G12C with a MRTX849 warhead and recruits the E3 ligase VHL, inducing rapid and sustained KRAS G12C degradation leading to suppression of MAPK signaling in both homozygous and heterozygous KRAS G12C cell lines.

HY-114398

BAY-293	Inhibitor	98.97%
BAY-293, a valuable chemical probe, blocks RAS activation via disruption of the KRAS-SOS1 interaction with an IC₅₀ of 21 nM. BAY-293 is a potent inhibitor of Son of Sevenless 1 (SOS1). SOS1 is the guanine nucleotide exchange factor (GEF) and activator of RAS.

HY-160699

DCC-3116	Inhibitor	99.25%
DCC-3116 is an orally active ULK1/2 inhibitor. DCC-3116 can inhibit autophagy in lung cancer cells by inhibiting KRAS^G12C signaling, thereby inhibiting the proliferation of lung cancer cells and exerting anti-cancer effects.

HY-148273

Setidegrasib	Inhibitor	99.65%
Setidegrasib (KRAS G12D inhibitor 17, ASP3082) is a PROTAC KRAS degrader (DC₅₀: 37 nM). Setidegrasib induces the degradation of G12D-mutation KRAS protein. Setidegrasib suppresses p-ERK, p-AKT, p-S6 levels in AsPC-1 cells. Setidegrasib exhibits anti-tumor activity in various cancer xenograft models in mice. Setidegrasib can be used for the study of KRAS(G12D)-mutated solid tumors. (Blue: VHL ligase ligand (HY-168699); Black: linker (HY-168698); Pink: G12D ligand (HY-168700)).

HY-153723

BI-2493	Inhibitor	99.79%
BI-2493 is a structural analogue of BI-2865 and a highly selective and orally active pan-KRAS inhibitor. BI-2493 can attenuate tumor growth. BI-2493 can be used for cancer iseases research.

HY-173632

AMG410	Inhibitor	98.50%
AMG410 is a non-covalent and selective pan-KRAS inhibitor with IC₅₀ values of 1-4 nM for KRAS G12D, KRAS G12V, and KRAS G13D. AMG410 shows greater than 100-fold selectivity against both HRAS and NRAS. AMG410 is a dual GTP(on)- and GDP(off)-state inhibitor (K_d(GDP-state) of 1 nM; K_d(GTP-state) of 22 nM). AMG410 blocks KRAS signaling in a cycling state-independent manner and also blocks proliferation in wildtype KRAS-amplified tumor cells. AMG410 can be used for the study of colorectal, pancreatic, and lung cancers.

HY-145926

MRTX0902	Inhibitor	99.75%
MRTX0902 is an orally active and potent SOS1 inhibitor with an IC₅₀ of 46 nM (WO2021127429A1; Example 12-10).

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