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]
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K-Ras Related Products (282)
Related Products (282)
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INCB159020
0 ImagesCat. No.: HY-168847CAS No.: 2923669-20-7INCB159020 is an orally active KRASG12D inhibitor with equivalent binding potency for the active GTP-bound and inactive GDP-bound forms of KRASG12D. INCB159020 can be used in the research of KRAS-driven cancers.
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IPS-06061
0 ImagesCat. No.: HY-170428CAS No.: 3064065-83-1IPS-06061 is an orally active molecular glue forming a ternary complex of CRBN-KRASG12D-IPS06061, degrading KRASG12D with a DC50 value lower than 500 nM. IPS-06061 shows a strong anti-tumor efficacy.
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RM-018
0 ImagesCat. No.: HY-141477CAS No.: 2641993-55-5RM-018 is a potent, functionally distinct tricomplex KRASG12C active-state inhibitor. RM-018 retains the ability to bind and inhibit KRASG12C/Y96D and could overcome resistance. RM-018 binds specifically to the GTP-bound, active [“RAS(ON)”] state of KRASG12C.
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KRAS G12D inhibitor 14
0 ImagesKRAS G12D inhibitor 14 is a potent KRAS G12D inhibitor with a KD of 33 nM for binding to KRAS G12D protein. KRAS G12D inhibitor 14 decreases the active form of KRAS G12D (KRAS G12D-GTP) but not KRAS G13D.
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KRAS inhibitor-24
0 ImagesCat. No.: HY-159474CAS No.: 3030576-47-4KRAS inhibitor-24 (compound 115c) is a pyridopyrimidine KRAS inhibitor, with an IC50 of < 100 nM for KRas G12V, KRas WT and KRas G12R.
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YN14
0 ImagesCat. No.: HY-155356Purity: 99.08%YN14 is a KRASG12C PROTAC degrader that recruits E3 ubiquitin ligase to induce the polyubiquitination and proteasomal degradation of KRASG12C. YN14 induces tumor cell apoptosis, cell cycle arrest, and cell migration inhibition. YN14 exhibits in vivo antitumor proliferative activity in tumor cell xenograft nude mice. YN14 can be used in cancer-related research.
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Atrovastatin-PEG3-FITC
0 ImagesAtrovastatin-PEG3-FITC (compound S31) is a KRAS-PDEδ interaction inhibitor. Atrovastatin-PEG3-FITC acts as a ligand in fluorescence anisotropy assay.
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(1R)-KRAS inhibitor-24
0 Images(1R)-KRAS inhibitor-24 (compound 115c) is a pyridopyrimidine KRAS inhibitor, with an IC50 of < 100 nM for KRas G12V, KRas WT and KRas G12R.
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CFL-120
0 ImagesCFL-120 is a potent KRasG12C inhibitor. CFL-120 shows an antiproliferative effect. CFL-120 shows anticancer activity. CFL-120 has the potential for the research of lung cancer.
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YK-8S
0 ImagesCat. No.: HY-159591CAS No.: 3060515-08-1YK-8S is a dual-targeted K-Ras (G12D/G12C) covalent inhibitor. YK-8S shows no significant binding to wild-type K-Ras and other mutants (G12R, G13D, Q61R/K). YK-8S exhibits anti-proliferative activity against H358 (G12C) and AGS (G12D) cells. YK-8S inhibits the phosphorylation of p-AKT/p-ERK in BaF3/G12D and G12C cells. YK-8S can be used for pancreatic cancer, colorectal cancer and other tumors with high incidence of G12D.
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PROTAC K-Ras Degrader-5
0 ImagesCat. No.: HY-168669CAS No.: 3052745-16-8PROTAC K-Ras Degrader-5 is a cereblon-based K-Ras PROTAC degrader with a DC50 of <100 nM for KRASG12D. PROTAC K-Ras Degrader-5 recruits KRASG12D to the cereblon E3 ubiquitin ligase complex for ubiquitination and subsequent proteasomal degradation. PROTAC K-Ras Degrader-5 suppresses pERK levels downstream of KRASG12D degradation in cancer cells. PROTAC K-Ras Degrader-5 reduces proliferation of cancer cells. PROTAC K-Ras Degrader-5 induces caspase 3/7 activity and cPARP, markers of apoptosis, in pancreatic cancer spheroids and tumors. PROTAC K-Ras Degrader-5 can be used for the research of pancreatic cancer and colorectal cancer.
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KRAS G12D inhibitor 3 TFA
0 ImagesKRAS G12D inhibitor 3 TFA is a KRAS G12D inhibitor with an IC50 of <500 nM. KRAS G12D inhibitor 3 TFA has antitumor effects (WO2022002102A1; compound 146). KRAS G12D inhibitor 3 (TFA) is a click chemistry reagent, it contains an Alkyne group and can undergo copper-catalyzed azide-alkyne cycloaddition (CuAAc) with molecules containing Azide groups.
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AZD4625
0 ImagesCat. No.: HY-146223Purity: 98.44%AZD4625 is an orally active, selective irreversible, covalent allosteric GTPase KRASG12C inhibitor with an IC50 of 3 nM. AZD4625 can inhibit the MAPK pathway (with decreased pCRAF, pMEK, and pERK) and the PI3K pathway (with decreased pAKT and pS6), and induce cell apoptosis. AZD4625 has no binding and inhibition of wild-type RAS or isoforms carrying non-KRASG12C mutations. AZD4625 can be used for the study of KRASG12C mutant non-small cell lung cancer.
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PROTAC K-Ras Degrader-2
0 ImagesCat. No.: HY-164365CAS No.: 3043670-74-9PROTAC K-Ras degrader-2 (compound 48) is a KRAS G12V PROTAC degrader with an IC50 of 20-200 nM for KRAS G12V/RAF1. PROTAC K-Ras degrader-2 degrades SW620 KRAS G12V with a DC50 of 1-10 nM. PROTAC K-Ras degrader-2 inhibits cell growth of SW620 3D cell with an IC50 of ≤10 nM. PROTAC K-Ras degrader-2 can be used for the study of colorectal cancer (CRC).
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Pan-RAS-IN-6
0 ImagesCat. No.: HY-168012CAS No.: 3054023-07-0Pan-RAS-IN-6 (compound 24) is an inhibitor targeting DUSP6, which reduces MAPK activation in the brain of the NCI-H1373-Luc model (DUSP6), at the same time, it shows significant tumor growth inhibition and tumor regression effects in the NSCLC brain metastasis mouse model. Pan-RAS-IN-6 shows high selectivity and strong inhibitory effects, especially in KRAS mutation-related signaling pathways, demonstrating varying inhibitory activity against different KRAS mutants and interacting proteins. The IC50 values for KRAS G12C, G12D, and G12V are 1.3 nM, 4.7 nM, and 0.3 nM, respectively.
