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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AM-8719
0 ImagesCat. No.: HY-187998CAS No.: 3034975-33-9AM-8719 is an orally active, blood-brain barrier-penetrant KRASG12C inhibitor. AM-8719 binds covalently to KRASG12C, inhibits SOS1-catalyzed GDP/GTP exchange, and suppresses downstream ERK phosphorylation. AM-8719 exhibits antiproliferative activity against KRASG12C tumor cells. AM-8719 can be used for the research of KRASG12C-positive cancers.
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KRAS inhibitor-15
0 ImagesCat. No.: HY-146545CAS No.: 2230873-75-1KRAS inhibitor-15 (compound 3-19) is a potent KRAS G12C inhibitor with an IC50 of 0.954 µM. KRAS inhibitor-15 shows p-ERK inhibition activities with IC50s of 2.03, >33.3 µM in MIA PaCA-2, A549 cells, respectively. KRAS inhibitor-15 has the potential for the research of pancreatic, colorectal, and lung cancers.
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KRAS G12D-IN-32
0 ImagesCat. No.: HY-179318CAS No.: 2885261-76-5KRAS G12D-IN-32 (Page 158) is a KRAS G12D inhibitor. KRAS G12D-IN-32 can be used to study adenocarcinoma, colorectal cancer, and non-small cell lung cancer.
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KRASG12C IN-17
0 ImagesCat. No.: HY-179403CAS No.: 2966924-23-0KRASG12C IN-17 is an orally active covalent KRASG12C inhibitor, showing strong inhibitory activity in KRASG12C-mutant cancer cells (NCI-H23 IC50 = 0.7 nM; NCI-H358 IC50 = 0.5 nM). KRASG12C IN-17 covalently and irreversibly binds to KRASG12C with > 96% modification efficiency in both GDP-bound and GMPPNP-bound conformations. KRASG12C IN-17 can be used for studies of KRAS-driven cancers, including colorectal cancer.
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YF135
0 ImagesCat. No.: HY-144323CAS No.: 2913177-53-2YF135 is a KRASG12C PROTAC degrader that mediates proteasomal degradation of KRASG12C in a reversible manner. In KRASG12C-mutant H358 and H23 lung cancer cells, the DC50 values of YF135 for KRAS degradation are 3.61 μM and 4.53 μM, respectively. YF135 attenuates the pERK signaling pathway in cancer cells. YF135 is applicable for lung cancer-related research.
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PPI stabilizer-1
0 ImagesCat. No.: HY-185217CAS No.: 2429876-60-6PPI stabilizer-1-1 (Compound 2) is a KRAS dimerizing agent. PPI stabilizer-1-1 dimerizes KRAS with a KD of 3.8 µM. PPI stabilizer-1-1 co-crystallizes with GCP-KRASG12D. PPI stabilizer-1 can be used for the research of KRAS-driven cancers.
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KRas G12C inhibitor 4
0 ImagesCat. No.: HY-112494CAS No.: 2206736-07-2KRas G12C inhibitor 1 is a compound that inhibits KRas G12C, extracted from patent US 20180072723 A1.
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KH-1
0 ImagesCat. No.: HY-P11901KH-1 is a KRASG12D/HDAC2 dual-target inhibitor with Kd values of 11.63 nM and 20.17 nM, respectively. KH-1 induces pancreatic cell apoptosis, cell cycle arrest, and inhibits cell proliferation, invasion and migration, as well as suppresses tumor growth in pancreatic cancer xenograft models. KH-1 can be used for the research of pancreatic cancer.
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KRAS G12C-IN-76
0 ImagesCat. No.: HY-181913CAS No.: 3023465-61-1KRAS G12C-IN-76 (Compound 39) is an orally active KRASG12C inhibitor. KRAS G12C-IN-76 inhibits the phosphorylation of ERK. KRAS G12C-IN-76 exhibits anticancer activity against pancreatic cancer.
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CH091138
0 ImagesCat. No.: HY-175025CH091138 is an orally active VHL-recruiting PROTAC degrader targeting KRASG12D, with a DC50 of 148.3 nM in HeLa cells. CH091138 inhibits cancer cell proliferation and tumor growth by mediating the ubiquitin-proteasome degradation of KRASG12D. CH091138 can be used in research related to pancreatic cancer and colorectal cancer.
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KD36
0 ImagesCat. No.: HY-179702KD36 is a selective KRAS-G12C inhibitor with an IC50 value of 0.92 μM. KD36 can inhibit the phosphorylation of ERK and AKT, induce the accumulation of reactive oxygen species (ROS), reduce mitochondrial membrane potential, thereby leading to apoptosis of KRAS-G12C mutant cells. KD36 can be used in the research of non-small cell lung cancer (NSCLC).
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(Rac)-Opnurasib
0 ImagesCat. No.: HY-139612BCAS No.: 2653201-38-6Synonyms: (Rac)-JDQ-443; (Rac)-NVP-JDQ443
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SOS1-IN-10
0 ImagesCat. No.: HY-144213CAS No.: 2758690-15-0SOS1-IN-10 is a potent SOS1 inhibitor with an IC50 of 13 nM for KRAS G12C-SOS1 (WO2022017519A1, compound 8).
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SOS1/KRAS-IN-2
0 ImagesCat. No.: HY-181807SOS1/KRAS-IN-2 (Compound 20) is a SOS1::KRASG12C protein-protein interaction inhibitor with a IC50 of 4.11 nM. SOS1/KRAS-IN-2 blocks the interaction between SOS1 and KRASG12C. SOS1/KRAS-IN-2 induces cell Apoptosis. SOS1/KRAS-IN-2 exhibits anticancer activity against colorectal cancer and tongue squamous cell carcinoma.
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NSC 373981
0 ImagesCat. No.: HY-182706CAS No.: 95455-02-0NSC 373981 is a CARD11 G4 stabilizer. NSC 373981 stabilizes the CARD11 G4 structure and inhibits CARD11 transcription in cells. NSC 373981 also inhibits BCL2 and MYC. NSC 373981 suppresses the transcription of KRAS and TERT. NSC 373981 exhibits anticancer activity against diffuse large B-cell lymphoma.
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KRAS G12C inhibitor 48
0 ImagesCat. No.: HY-146061CAS No.: 3033236-94-8KRAS G12C inhibitor 48 (compound 6e) is a potent KRAS G12C inhibitor with an IC50 of 639.91 nM. KRAS G12C inhibitor 48 (0-50 µM) shows anti-proliferative activity with IC50s of 0.796, 6.33, 16.14 µM for H358, H23, A549 cells, respectively.
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Eras-4001-d6
0 ImagesCat. No.: HY-175870SCAS No.: 3024881-00-0Eras-4001-d6 is a deuterated form of Eras-4001 (HY-175870). Eras-4001 is a potent, orally active pan-KRAS inhibitor with Kd values of 110, 13 and 39 pM against wild-type, G12D and G12V mutant KRAS, respectively, and exhibits selectivity toward wild-type HRAS and NRAS. Eras-4001 inhibits ERK1/2 phosphorylation and cell viability in cancer cells. Eras-4001 induces tumor growth inhibition and regression in subcutaneous xenograft models. Eras-4001 can be used in research on non-small cell lung cancer, ovarian cancer, etc.
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PHI-501
0 ImagesCat. No.: HY-153858CAS No.: 2470433-36-2PHI-501 is a dual inhibitor targeting RAF/DDR. PHI-501 exhibits significant anti-proliferative effects in melanoma cell lines and significantly inhibits the colony formation of drug-resistant cells. PHI-501 strongly inhibits ERK and AKT phosphorylation. PHI-501 downregulates the gene sets in drug-resistant cells of TNFA-NFKB, IL6-JAK-STAT3, and KRAS signaling pathways as well as the epithelial-mesenchymal transition (EMT) signaling pathways. PHI-501 demonstrates significant anti-tumor effects in the SK-MEL3DR xenograft model. PHI-501 can be used for research on the problem of drug resistance in melanoma.
