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 (287)
Related Products (287)
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KRAS G12C inhibitor 44
0 ImagesCat. No.: HY-142946CAS No.: 2927439-07-2KRAS G12C inhibitor 44 (compound 54) is a potent and orally active KRAS G12C inhibitor. KRAS G12C inhibitor 44 shows anti-proliferation activities with IC50s of 0.016, 0.028 µM in MIA PaCA-2, H358 cells, respectively. KRAS G12C inhibitor 44 shows antitumor effects in vivo.
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RMC-8839
0 ImagesCat. No.: HY-184892CAS No.: 2953305-55-8RMC-8839 is an orally active selective RAS (ON) G13C inhibitor with a Ki value of 28.3 nM. RMC-8839 disrupts the interaction between KRASG13C and RAF1 (RBD). RMC-8839 inhibits RAS-MAPK pathway signaling by reducing DUSP6 mRNA levels and pERK levels. RMC-8839 induces cytotoxicity, apoptosis (apoptosis) and antiproliferative effects in KRASG13C-mutated cells. RMC-8839 induces tumor stasis or regression in mice. RMC-8839 can be used in research related to non-small cell lung cancer.
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KRAS G12C inhibitor 52
0 ImagesCat. No.: HY-147633CAS No.: 2761204-87-7KRAS G12C inhibitor 52 (Compound 7) is a KRAS G12C inhibitor.
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KRAS inhibitor-12
0 ImagesCat. No.: HY-146533CAS No.: 2230874-00-5KRAS inhibitor-12 (compound 6-1) is a potent KRAS G12C inhibitor with an IC50 of 0.537 µM. KRAS inhibitor-12 shows p-ERK inhibition activities with IC50s of 1.3, 3.7 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-12 has the potential for the research of pancreatic, colorectal, and lung cancers.
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SOS1-IN-7
0 ImagesCat. No.: HY-144211CAS No.: 2755415-30-4SOS1-IN-7 (compound 18-p1) is a potent SOS1 inhibitor with IC50s of 20 and 67 nM for SOS1-G12D and SOS1-G12V, respectively.
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KRAS G12C inhibitor 46
0 ImagesCat. No.: HY-142948CAS No.: 2573769-23-8KRAS G12C inhibitor 46 (compound WX003) is a potent KRAS G12C inhibitor.
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KRAS inhibitor-23
0 ImagesCat. No.: HY-160220SCAS No.: 2641747-55-7
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KRASG12D-IN-5
0 ImagesCat. No.: HY-174243CAS No.: 2933935-13-6KRASG12D-IN-5 (Compound 241) is an orally active KRAS(G12D) inhibitor with an IC50 of 11 nM. KRASG12D-IN-5 has potent anticancer activity with no significant cytotoxicity against BxPC-3 (WT), KRAS mutation AsPC-1 (G12D) and MIAPaCa-2 cells (G12C) with CC50s of 10.37, 0.76 and 0.3 μM, respectively. KRASG12D-IN-5 can be used for cancer research, such as lung, pancreatic and colorectal cancer.
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KRAS-IN-48 free base
0 ImagesCat. No.: HY-179300CAS No.: 3074833-86-3KRAS-IN-48 free base (Compound 1-01) is a mutant KRAS inhibitor, with Kd values of 2.58 nM and 5.49 μM for KRAS G12D and KRAS G12V, respectively. KRAS-IN-48 free base affects pERK expression in cells harboring KRAS G12D and KRAS G12V mutations, with IC50 values of 1.1 μM and 1.51 μM, respectively. KRAS-IN-48 free base can be used in the research of cancer.
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NTLiverTac PDE6D degrader-1
0 ImagesCat. No.: HY-174379NTLiverTac PDE6D degrader-1 is a PDE6D NTLiverTac degrader with a DC50 of 4.09 μM. NTLiverTac PDE6D degrader-1 is formed by conjugating a PDE6D PROTAC degrader with the NTCP ligand Cholic acid (HY-N0324). NTLiverTac PDE6D degrader-1 triggers the ubiquitin-proteasome system-mediated degradation process by forming a complex with PDE6D and MDM2, inducing proteasome-dependent and NTCP-dependent degradation. NTLiverTac PDE6D degrader-1 inhibits PDE6D-dependent KRAS trafficking and suppresses KRAS-related oncogenic signaling cascades. NTLiverTac PDE6D degrader-1 inhibits the activation of the PI3K/AKT/mTOR signaling pathway and induces cellular Apoptosis. NTLiverTac PDE6D degrader-1 enters cancer cells via NTCP-mediated endocytosis. NTLiverTac PDE6D degrader-1 can be used in the research of hepatoblastoma (MDM2 ligand: (4R,5S)-Nutlin carboxylic acid (HY-128836); NTCP ligand: Cholic acid (HY-N0324); PDE6D ligand: Sorafenib (HY-10201)).
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BRSD-143
0 ImagesCat. No.: HY-184010CAS No.: 3101973-42-3BRSD-143 is an orally active KRASG12D inhibitor, with a Kd value of 0.003 nM for KRASG12D and 0.024 nM for KRASG12V. BRSD-143 inhibits the activity of phosphorylated ERK in KRAS-mutated cells. BRSD-143 induces tumor regression in ovarian cancer xenograft mouse models. BRSD-143 can be used for the research of KRAS-mutated cancers.
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pan-KRAS-IN-13
0 ImagesCat. No.: HY-162446CAS No.: 3033637-76-9pan-KRAS-IN-13 (compound 2) is a potent inhibitor of KRAS, with IC50s of 2.75 nM and 2.89 nM for G12D and G12V, respectively
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KRAS G12D ligand-2
0 ImagesCat. No.: HY-168700KRAS G12D ligand-2 is a Ligand for Target Protein for PROTAC. KRAS G12D ligand-2 can be used to synthesize Setidegrasib (HY-148273).
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Spiclomazine hydrochloride
0 ImagesCat. No.: HY-122152CAS No.: 27007-85-8Synonyms: APY-606; Clospirazine hydrochloride
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KRAS degrader-1
0 ImagesCat. No.: HY-153880CAS No.: 2795275-59-9KRAS degrader-1 is a potent KRAS degrader. KRAS degrader-1 targets specific proteins for degradation via the autophagy-lysosomal degradation pathway. KRAS degrader-1 is suitable for use in cancer research. (Blue: KRAS G12C-IN-72 (HY-128414); Black: Linker (HY-175587); Pink: 5-Iodoindolin-2-one (HY-76986); Blue + Black: KRAS ligand-Linker Conjugate 7 (HY-175586)).
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AMG410 diTFA
0 ImagesCat. No.: HY-173632ACAS No.: 3040175-18-3AMG410 diTFA 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 diTFA shows greater than 100-fold selectivity against both HRAS and NRAS. AMG410 diTFA is a dual GTP(on)- and GDP(off)-state inhibitor (Kd(GDP-state) of 1 nM; Kd(GTP-state) of 22 nM). AMG410 diTFA blocks KRAS signaling in a cycling state-independent manner and also blocks proliferation in wildtype KRAS-amplified tumor cells. AMG410 diTFA can be used for the study of colorectal, pancreatic, and lung cancers.
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KRAS G12C inhibitor 47
0 ImagesCat. No.: HY-146537CAS No.: 2253119-24-1KRAS G12C inhibitor 47 (compound 8-1-1) is a potent KRAS G12C inhibitor with an IC50 of 0.172 µM. KRAS G12C inhibitor 47 shows p-ERK inhibition activities with IC50s of 0.046, 69.8 µM in MIA PaCA-2, A549 cells, respectively. KRAS G12C inhibitor 47 has the potential for the research of pancreatic, colorectal, and lung cancers.
