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 59
0 ImagesCat. No.: HY-153899CAS No.: 2914919-88-1KRAS G12C inhibitor 59 is a KRAS G12C inhibitor with anticancer effects (WO2023036282A1, compound II).
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KRAS G12C inhibitor 23
0 ImagesCat. No.: HY-145020CAS No.: 2735721-00-1KRAS G12C inhibitor 23 is a KRAS G12C inhibitor. KRAS G12C inhibitor 23 inhibits H358 cells with an IC50 of 491 nM (WO2021218939A1, compound 1).
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KRAS G12C inhibitor 25
0 ImagesCat. No.: HY-145022CAS No.: 2734060-73-0KRAS G12C inhibitor 25 is a KRAS G12C inhibitor. KRAS G12C inhibitor 25 inhibits SOSl-assisted GDP/GTP exchanging activity of KRAS-G12C mutant (IC50=0.48 nM). From WO2021216770A1 compound 3.
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pan-KRAS-IN-3
0 ImagesCat. No.: HY-156555CAS No.: 2875116-29-1pan-KRAS-IN-3 (Example 84) is a pan-KRAS inhibitor. pan-KRAS-IN-3 can be used for research of cancers. pan-KRAS-IN-3 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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KRAS G12D-IN-37
0 ImagesCat. No.: HY-183355KRAS G12D-IN-37 is a KRASG12D inhibitor. KRAS G12D-IN-37 shows antiproliferative activity against KRASG12D mutant tumor cells and minimal cytotoxicity toward normal cells. KRAS G12D-IN-37 binds stably to KRASG12D via hydrogen bond interactions with residues His 95, Arg 68, and Asp 12, and inhibits downstream ERK/AKT signaling pathways. KRAS G12D-IN-37 elevates ROS levels, induces apoptosis, disrupts mitochondrial membrane potential. KRAS G12D-IN-37 downregulates the level of anti-apoptotic protein Bcl-2, and upregulates the levels of pro-apoptotic proteins Bax and caspase 3. KRAS G12D-IN-37 can be used for the research of cancer, such as gastric adenocarcinoma and colorectal cancer.
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pan-KRAS-IN-20
0 ImagesCat. No.: HY-182994CAS No.: 3111803-46-1
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KRAS G12D-IN-35
0 ImagesCat. No.: HY-180885SKRAS G12D-IN-35 (example 7) is a potent and orally active KRAS G12D inhibitor. KRAS G12D-IN-35 suppresses p-ERK in AGS cells and potently inhibits the proliferation of various KRAS G12D-mutant cancer cell lines. KRAS G12D-IN-35 inhibits tumor growth in HPAC and GP2D mouse models. KRAS G12D-IN-35 can be used for cancer research, such as pancreatic and colorectal cancer.
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KRAS-IN-65
0 ImagesCat. No.: HY-189666CAS No.: 3101978-77-9KRAS-IN-65 is an orally active KRAS inhibitor. KRAS-IN-65 inhibits KRAS G12D/G12V signaling with IC50 values of 20 nM and 5 nM, respectively. KRAS-IN-65 exhibits reduced glucuronidation and intestinal stability. KRAS-IN-65 produces limited tumor growth inhibition in xenograft models. KRAS-IN-65 can be used for cancer-related research, such as non-small cell lung cancer and colorectal cancer.
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PCA-IN-1
0 ImagesCat. No.: HY-183625PCA-IN-1 is a polyisoprenylated cysteinyl amide (PCA) inhibitor that acts on multiple KRAS mutant subtypes. PCA-IN-1 dissociates KRAS4B from its transport chaperones, prevents its localization to the plasma membrane, and blocks downstream oncogenic signaling pathways. PCA-IN-1 inhibits colony formation of KRAS-mutant lung cancer cells, induces sustained long-term growth inhibition, and suppresses cell migration. PCA-IN-1 is applicable to the research of KRAS-mutant lung cancer.
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KRAS-IN-48
0 ImagesCat. No.: HY-179300ACAS No.: 3074833-87-4KRAS-IN-48 (Compound 1-01) is a KRAS mutant inhibitor, with Kd values of 2.58 nM and 5.49 μM for KRAS-G12D and KRAS-G12V, respectively. KRAS-IN-48 can be used in the research of cancer.
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KRAS G12C inhibitor 57
0 ImagesCat. No.: HY-151968CAS No.: 2821863-70-9
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KRASG12C IN-20
0 ImagesCat. No.: HY-182883KRASG12C IN-20 is an orally potent KRASG12C inhibitor with an EC50 of 3.9 nM. KRASG12C IN-20 covalently modifies KRASG12C in its inactive GDP-bound state and locks it to block oncogenic signal transduction. KRASG12C IN-20 exhibits significant activity in lung adenocarcinoma xenograft models. KRASG12C IN-20 can be used for research related to lung adenocarcinoma.
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KRAS-IN-43
0 ImagesCat. No.: HY-176250KRAS-IN-43 (Compound 9) is a pan-KRAS inhibitor with IC50 values of 0.15 μM, 0.14 μM, and 0.47 μM against KRASG12V, KRASG12C and wild-type KRAS, respectively. KRAS-IN-43 disrupts the interaction between KRAS and cRAF, and inhibits ERK phosphorylation. KRAS-IN-43 is promising for research of KRAS mutation-related cancers (such as pancreatic cancer, colorectal cancer, and lung cancer).
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KRAS G13D-IN-2
0 ImagesCat. No.: HY-179452KRAS G13D-IN-2 (compound 8B) is a potent orally active KRAS G13D inhibitor with IC50 values of 1.95 μM (HCT-116G13D) and 2.16 μM (HCT-15G13D). KRAS G13D-IN-2 induces G1-phase arrest and mitochondrial membrane depolarization. KRAS G13D-IN-2 induces senescence through CDK6/TWIST1 inhibition. KRAS G13D-IN-2 inhibits tumor growth in murine models. KRAS G13D-IN-2 can be used for KRASG13D-mutant colorectal cancer research.
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KRAS inhibitor-37
0 ImagesCat. No.: HY-169311CAS No.: 3058573-95-5KRAS inhibitor-37 is a KRAS inhibitor. KRAS inhibitor-37 inhibits the activity of KRASG12C, KRASG12D, and KRASG12V receptors. KRAS inhibitor-37 can be used in cancer research.
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KRAS-IN-56
0 ImagesCat. No.: HY-182411CAS No.: 2375482-34-9KRAS-IN-56 (Compound 18) is a KRAS inhibitor with an EC50 of 33 μM. KRAS-IN-56 inhibits the interaction between GTP-KRAS and SOS1. KRAS-IN-56 induces a decrease in p-ERK levels. KRAS-IN-56 can be used in research related to lung cancer.
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JOSD2-IN-1
0 ImagesCat. No.: HY-179058JOSD2-IN-1 (Compound 31) is a covalent JOSD2 inhibitor with an IC50 value of 1.95 μM. JOSD2-IN-1 inhibits JOSD2, thereby down-regulating KRAS expression. JOSD2-IN-1 exhibits significant anti-proliferative activity against HCT116 cells. JOSD2-IN-1 can be used for research on colorectal cancer.
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KRAS G12D-IN-36
0 ImagesCat. No.: HY-180920KRAS G12D-IN-36 (Compound 53a) is a highly selective and orally active KRAS-G12D inhibitor with an IC50 of 1.63 nM. KRAS G12D-IN-36 effectively inhibits p-ERK with an IC50 of 8.4 nM. KRAS G12D-IN-36 shows potent anti-proliferative activity against AsPC-1 cells. KRAS G12D-IN-36 can be used for research on pancreatic cancer.
