K-Ras
K-Ras (KRAS) is a small GTPase that functions as a molecular switch within the RAS/MAPK signaling network, cycling between inactive GDP-bound and active GTP-bound states to regulate cell proliferation, differentiation, and survival[1][2]. Mechanistically, activated KRAS transduces signals from cell-surface receptors to downstream effectors, including the MAPK/ERK and PI3K/AKT pathways, thereby coordinating cellular growth and stress-response programs[1][3]. Oncogenic mutations impair GTP hydrolysis and maintain persistent KRAS signaling, resulting in sustained activation of proliferative pathways that contribute to tumor initiation, progression, and therapeutic resistance across multiple cancer types, particularly pancreatic ductal adenocarcinoma, colorectal cancer, and non-small cell lung cancer[2][3][4]. In disease models, mutant KRAS also reshapes the tumor microenvironment through inflammatory and immune-regulatory signaling, further supporting tumor development and immune evasion[3][2]. Compared with the related RAS isoforms HRAS and NRAS, KRAS is the most frequently altered RAS family member in human cancer and accounts for the majority of oncogenic RAS mutations, highlighting its distinct biological and clinical importance[2][5]. For experimental applications, the development of mutation-selective inhibitors, especially KRAS^G12C^ inhibitors, has established a tractable platform for studying KRAS-dependent signaling and therapeutic resistance mechanisms, although resistance remains a major challenge for long-term clinical efficacy[2][5].
References:
- [1]. K-Ras gene information.
- [2]. Huang L, et al. KRAS mutation: from undruggable to druggable in cancer. Signal Transduct Target Ther. 2021 Nov 15;6(1):386. [Content Brief]
- [3]. Uniyal P, et al. KRAS Mutations in Cancer: Understanding Signaling Pathways to Immune Regulation and the Potential of Immunotherapy. Cancers (Basel). 2025 Feb 25;17(5):785. [Content Brief]
- [4]. Suda K, et al. Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation. Cancer Metastasis Rev. 2010 Mar;29(1):49-60. [Content Brief]
- [5]. Riedl JM, et al. Emerging landscape of KRAS inhibitors in cancer treatment. Cancer Cell. 2026 Mar 9;44(3):471-497. [Content Brief]
-
K-Ras Related Products (282)
Related Products (282)
-
K20
0 ImagesCat. No.: HY-115907K20 is a potent and selective KRas G12C inhibitor with an IC50 of 1.16 µM. K20 shows anticancer activity in H358 cells (IC50= 0.78 µM). K20 decreases the levels of phosphorylated Erk and leads to cancer cell apoptosis. K20 suppresses NCI-H358 tumor growth with a TGI of 41% without causing obvious toxicity.
-
(R)-ACBI-4
0 ImagesCat. No.: HY-176792ACAS No.: 3097973-97-9
-
KRAS G12D inhibitor 7
0 ImagesCat. No.: HY-139911CAS No.: 2648552-34-3KRAS G12D inhibitor 7 is an inhibitor of KRAS G12D. KRAS G12D inhibitor 7 can be used for the research of cancer.
-
KRAS G12C inhibitor 61
0 ImagesCat. No.: HY-156549CAS No.: 2300967-40-0KRAS G12C inhibitor 61 (Example 3) inhibits phospho-ERK 1/2 in MIA PaCa-2 cells with an IC50 value of 9 nM. KRAS G12C inhibitor 61 can be used for research of pancreatic, colorectal, and lung cancers.
-
KRAS G12D inhibitor 16
0 ImagesCat. No.: HY-148260CAS No.: 2648221-12-7KRAS G12D inhibitor 16 is a KRAS G12D inhibitor. KRAS G12D inhibitor 16 has inhibitory activity against KRAS G12D and KRAS G12D mutation with IC50 value of 0.7 nM and 0.35 μM, respectively. KRAS G12D inhibitor 16 can be used for the research of many malignant tumor, such as pancreatic ductal adenocarcinomas (PDAC), colon and rectal carcinomas (CRC), non-small cell lung carcinomas (NSCLC).
-
Zecdarasib
0 ImagesCat. No.: HY-187874CAS No.: 3080960-85-3Zecdarasib is a Kirsten rat sarcoma virus oncogene homolog (KRAS) inhibitor with antitumor activity. Zecdarasib can be used in tumor-related research.
-
KRAS ligand 6
0 ImagesCat. No.: HY-189223KRAS ligand 6 (Compound 37) is a KRAS ligand. KRAS ligand 6 can be used as a Ligand for Target Protein for PROTAC to synthesize KRAS PROTAC degraders, such as RP04340 (HY-189222). KRAS ligand 6 can be used for research on KRAS-driven cancers, including pancreatic ductal adenocarcinoma, colorectal cancer, and lung adenocarcinoma.
-
KRAS G12C inhibitor 54
0 ImagesCat. No.: HY-147635CAS No.: 2765580-17-2KRAS G12C inhibitor 54 (Compound 1) is a KRAS G12C inhibitor.
-
pan-KRAS-IN-16
0 ImagesCat. No.: HY-164645CAS No.: 2368246-78-8pan-KRAS-IN-16 (Compound 3344) is an anti-RAS small molecule derived from an intracellular antibody fragment with pan-RAS-effector protein-protein interaction inhibitor properties. pan-KRAS-IN-16 binds to a hydrophobic pocket near to the effector-binding switch regions of RAS. pan-KRAS-IN-16 prevents endogenous RAS-dependent signaling in tumor cell lines.
-
PQ32
0 ImagesCat. No.: HY-175265PQ32 is an antitumor agent that targets c-MYC Pu27 and KRAS G-quadruplexes. PQ32 inhibits tumor cell proliferation, arrests the cell cycle at the G2 phase, and induces apoptosis. PQ32 inhibits the expression of c-MYC and KRAS genes. PQ32 can inhibit tumor growth in mice and is used in the study of lymphoma, breast cancer, lung cancer, hepatocellular carcinoma, colorectal cancer, and other cancers.
-
SOS1-IN-9
0 ImagesCat. No.: HY-144207CAS No.: 2758900-76-2SOS1-IN-9 is a potent SOS1 inhibitor with an IC50 of 116.5 nM for SOS1-KRAS G12C (WO2022028506A1, compound 302).
-
KRAS G12C-IN-71
0 ImagesCat. No.: HY-180298CAS No.: 2080446-99-5KRAS G12C-IN-71 (Compound 11) is a covalent G12C KRAS inhibitor with a Ki of 380 nM. KRAS G12C-IN-71 can be used in the research of non-small cell lung cancer.
-
KRAS G12C-IN-70
0 ImagesCat. No.: HY-174851CAS No.: 2923865-76-1KRAS G12C-IN-70 is a selective KRAS G12C mutant inhibitor. KRAS G12C-IN-70 blocks KRAS G12C-mediated downstream signaling pathways (e.g., RAF-MEK-ERK) and inhibits tumor cell proliferation. KRAS G12C-IN-70 is promising for research of KRAS G12C mutation-related tumors (such as non-small cell lung cancer, colorectal cancer).
-
SL43
0 ImagesCat. No.: HY-183365SL43 is an orally active and potent SOS1 inhibitor with a Kd of 0.16 μM. SL43 disrupts SOS1-KRAS interaction, inhibits SOS1-mediated nucleotide exchange on KRAS mutants, and suppresses RAS-MAPK signaling. SL43 exerts antiproliferative activity against KRAS-mutant cancer cells, induces early apoptosis and G1 phase cell cycle arrest, and reduces phosphorylated MEK and ERK levels. SL43 suppresses tumor growth in a colorectal cancer xenograft model.
-
SS-3091
0 ImagesCat. No.: HY-178042CAS No.: 2756257-56-2SS-3091 is a pan-KRas inhibitor active across KRasG12D, KRasG12C, KRasG12V, KRasG12S mutants, with minimal effects on non-KRas-driven cancer cells. SS-3091 binds to the KRas·ARaf interaction interface, destabilizes the complex, and attenuates KRas activity. SS-3091 suppresses phosphorylation of S6K, Akt, and ERK. SS-3091 reduces proliferation and decreases colony formation of cancer cells bearing KRasG12 mutations. SS-3091 can be used for the research of KRas-driven cancers.
-
KRAS inhibitor-17
0 ImagesCat. No.: HY-146475CAS No.: 2230873-65-9KRAS inhibitor-17 (compound 3-9) is a potent KRAS G12C inhibitor with an IC50 of 3.37 µM. KRAS inhibitor-17 shows p-ERK inhibition activities with IC50s of 9.25, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-17 has the potential for the research of pancreatic, colorectal, and lung cancers.
-
KRAS-IN-58
0 ImagesCat. No.: HY-182749KRAS-IN-58 is a KRAS inhibitor with a IC50 of 0.223 μM against KRASG12D. KRAS-IN-58 binds to KRASG12C and KRASG12D proteins, and reduces the levels of phosphorylated Raf1, AKT and ERK in pancreatic cancer cells. KRAS-IN-58 can be used for the research of pancreatic cancer.
-
RAS GTPase-IN-3
0 ImagesCat. No.: HY-189129RAS GTPase-IN-3 is a RAS GTPase inhibitor that targets multiple KRAS-Q61 mutant variants. RAS GTPase-IN-3 binds to the switch II pocket of GTP-bound KRAS-Q61R, positions its side-chain imidazole group near the GTP γ-phosphate, and accelerates GTP hydrolysis of KRAS-Q61. RAS GTPase-IN-3 inhibits Sos-catalyzed nucleotide exchange on GTP-bound KRAS. RAS GTPase-IN-3 only activates GTP hydrolysis of HRAS-Q61R/Q95H and NRAS-Q61R/L95H mutant proteins. RAS GTPase-IN-3 can be applied in research related to cancers driven by KRAS-Q61 mutations.
