2. Signaling Pathways
  3. GPCR/G Protein
    MAPK/ERK Pathway
  4. Ras
  5. H-Ras Isoform

H-Ras

H-Ras (HRAS) is a small GTPase that functions as a GDP/GTP-regulated molecular switch linking activated cell-surface receptors to intracellular signaling networks that control cell proliferation, differentiation, survival, and migration[4][5]. Mechanistically, H-Ras cycles between inactive GDP-bound and active GTP-bound states and transmits signals through major effector pathways, including the RAF-MEK-ERK and PI3K-AKT cascades, thereby coordinating growth factor-dependent cellular responses[6][1]. In disease contexts, activating HRAS mutations promote persistent downstream signaling and contribute to multiple human malignancies, with notable involvement in bladder, thyroid, head and neck, and oral squamous cell carcinomas[7][2]. Compared with related Ras isoforms, H-Ras, K-Ras, and N-Ras share highly conserved G-domains but differ substantially within their C-terminal hypervariable regions, which determine membrane trafficking, subcellular localization, and isoform-specific signaling outputs[4][8]. H-Ras is further distinguished by its dynamic palmitoylation-dependent trafficking between the plasma membrane and endomembrane compartments, enabling spatially restricted signal transduction and context-dependent biological effects[8][3]. These isoform-specific properties make H-Ras an important experimental model for dissecting Ras signaling compartmentalization and oncogenic network regulation[4][8]. For experimental and translational applications, H-Ras remains a particularly tractable therapeutic target because its membrane localization depends on farnesylation, and pharmacological farnesyltransferase inhibitors such as tipifarnib can suppress H-Ras-dependent signaling in selected tumor models[2][9].

H-Ras Related Products (4):

Cat. No. Product Name Effect Purity
  • HY-156498
    RMC-7977
    		Inhibitor 99.48%
    RMC-7977 is an orally active triple-complex RAS inhibitor that can simultaneously bind to cyclophilin A (CYPA) (Kd = 195 nM) and KRAS (G12V) (Kd = 292 μM). It exhibits broad-spectrum inhibitory activity against KRAS, NRAS, and HRAS proteins and their various wild-type and mutant variants. RMC-7977 induces apoptosis by inhibiting the phosphorylation of ERK, CRAF, and RSK, as well as increasing PARP cleavage. This leads to tumor regression, reduces resistance in KRASG12C cancer models, and demonstrates good tolerability across various RAS cancer models.
  • HY-15716
    Kobe0065
    		Inhibitor 99.93%
    Kobe0065 is a novel and effective inhibitor of Ras-Raf interaction, competitively inhibiting the binding of H-Ras·GTP to c-Raf-1 RBD with a Ki value of 46±13 μM.
  • HY-116428
    L-744832
    		Modulator
    L-744832 is a farnesyl transferase inhibitor. L-744832 effectively inhibits the farnesylation of H-Ras and N-Ras, but has little effect on K-Ras treatment. L-744832 not only directly targets the oncogenic pathway by inhibiting Ras farnesylation, but also enhances radiosensitivity by restoring TGF-β signaling through epigenetic reprogramming. L-744832 can induce cell cycle arrest and apoptosis. L-744832 can be used in combination therapy studies for Ras-driven tumors such as pancreatic cancer.
  • HY-164645
    pan-KRAS-IN-16
    		Inhibitor
    pan-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.