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Results for "

Cancer therapy resistance

" in MedChemExpress (MCE) Product Catalog:

7

Inhibitors & Agonists

1

Isotope-Labeled Compounds

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Click Chemistry

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-175633
    ML210-ansaFc

    		Glutathione Peroxidase Ferroptosis Reactive Oxygen Species (ROS) Cancer
    ML210-ansaFc (Compound III-13) is a covalent GPX4 inhibitor with a [3]-ferrocenophane group (IC50 of 3.4 μM). ML210-ansaFc potently induces ferroptosis by increasing the level of ROSand promoting lipid peroxidation (LPO) in cancers cells. ML210-ansaFc has an anticancer activity and suppresses tumor growth in tumor 3D spheroids. ML210-ansaFc can be used for cancer therapy resistance research .
    ML210-ansaFc
  • HY-106072
    Vinzolidine

    LY 104208

    		 Microtubule/Tubulin Cancer
    Vinzolidine is a semisynthetic derivative of the catharanthus alkaloid. Vinzolidine exerts its cytotoxic effect on tumor cells by interfering with microtubulin polymerization, thereby inhibiting cell division. Vinzolidine can be utilized in research to investigate synergistic effects when combined with other chemotherapeutic agents or biologic therapies, as well as to study cancer cells' tolerance or resistance to these treatments, and to explore approaches to overcome such obstacles .
    Vinzolidine
  • HY-172922
    FGFR-IN-19

    		FGFR Cancer
    Arg-IN-1 is a selective Arginine (Arg)-targeting covalent inhibitor with IC50s of 9.7 nM and 30.4 nM for FGFR2 and FGFR3,respectively. Arg-IN-1 has the potential to avoid FGFR1/4-targeted toxicity as well as conquer acquired on-target resistance, potential for FGFR-targeting cancer therapy .
    FGFR-IN-19
  • HY-164473
    DETD-35

    		ERK Akt STAT Apoptosis Cancer
    DETD-35 is an inhibitor of the MEK-ERK, Akt, and STAT3 signaling pathways, which promotes cancer cell apoptosis (Apoptosis) and reduces cancer cell resistance to Vemurafenib (HY-12057). The IC50 values of DETD-35 against wild-type and mutant melanoma cell lines B16-F10, MeWo, SK-MEL-2, A2058c, and A375c are 2.7, 6.0, 3.9, 3.1, and 2.5 μM, respectively. DETD-35 holds promise for research in the field of anti-melanoma therapy .
    DETD-35
  • HY-116497
    PH11

    		FAK Cancer
    PH11 is a novel focal adhesion kinase (FAK) inhibitor that rapidly induces apoptosis in TRAIL-resistant PANC-1 cells when combined with TRAIL, but has no effect on normal human fibroblasts. The study found that PH11 downregulates c-FLIP through inhibition of FAK and phosphatidylinositol-3-kinase (PI3K)/AKT pathways, thereby restoring the TRAIL apoptotic pathway, suggesting that this combination therapy may provide an attractive therapeutic strategy for the safe and effective treatment of pancreatic cancer. PH11 selectively inhibits c-FLIP expression by modulating upstream signaling pathways and may represent an innovative therapeutic strategy. Although further work is needed to fully elucidate the mechanism of PH11-induced TRAIL sensitization, we believe that our results will provide a new approach to target c-FLIP without the risk of interfering with caspase-8 processing, which could potentially lead to TRAIL resistance. This study also suggests a role for the FAK/AKT signaling pathway in regulating c-FLIP expression in TRAIL-induced apoptosis, and this understanding will provide important clues to control the resistance mechanism to optimize the potential of TRAIL-based pancreatic cancer treatment.
    PH11
  • HY-176785S
    MCB-294

    		Ras Apoptosis p38 MAPK Caspase TNF Receptor Cancer
    MCB-294 is a dual-state pan-KRAS inhibitor that selectively inhibits KRAS over NRAS and HRAS. MCB-294 capable of binding both the active (GTP-bound) and inactive (GDP-bound) forms of KRAS with Kds of approximately 1 pM and 10 nM, respectively. MCB-294 broadly impairs the growth of hTERT-HPNE cells expressing G12D, G12C, G12V, G12S, G13D, and wild-type KRAS, with IC50s of approximately 700 nM. MCB-294 induces irreversible apoptosis in KRAS-mutated tumors. MCB-294 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-294 can be used for the study of pancreatic cancer, colorectal cancer and lung cancer .
    MCB-294
  • HY-176786
    MCB-36

    		PROTACs Ras Apoptosis PERK p38 MAPK Caspase TNF Receptor Cancer
    MCB-36 is a VHL-recruiting pan-KRAS PROTAC degrader without affecting KRAS transcription. MCB-36 exhibits minimal effects on HRAS and NRAS protein levels. MCB-36 binds to the GDP-loaded state of G12D, G12C, G12V, and wild-type KRAS with high affinities Kd ≈ 1 pM). MCB-36 decreases p-ERK levels, leading to cell apoptosis. MCB-36 effectively suppress KRAS G12C inhibitor-resistant cancer cells and remodel the tumor immune microenvironment. MCB-36 can be used for the study of colorectal cancer and lung cancer (Pink: Target protein ligand; Blue: E3 ligand (HY-112078); Black: Linker (HY-W091879)) .
    MCB-36

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