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Pathways Recommended: Stem Cell/Wnt Cell Cycle/DNA Damage
Results for "

cell death inhibition

" in MedChemExpress (MCE) Product Catalog:

14

Inhibitors & Agonists

1

Biochemical Assay Reagents

3

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-138201
    IM-93

    		Ferroptosis Cardiovascular Disease
    IM-93 inhibits ferroptosis and NETosis with an IC< sub>50 of 0.45 µM for cell death inhibition .
    IM-93
  • HY-N6036
    Ganoderic acid F
    1 Publications Verification

    		 Others Cancer
    Ganoderic acid F is a ganoderic acid. Ganoderic acid F exhibits antitumor and antimetastatic activities through inhibition of angiogenesis and alteration of proteins involving cell proliferation and/or cell death, carcinogenesis, oxidative stress, calcium signaling, and endoplasmic reticulum stress .
    Ganoderic acid F
  • HY-134904
    RMC-6272
    1 Publications Verification

    RM-006

    		 mTOR Cancer
    RMC-6272 (RM-006) is a bi-steric mTORC1-selective inhibitor. RMC-6272 exhibits potent and selective (> 10-fold) inhibition of mTORC1 over mTORC2. RMC-6272 shows improved inhibition of mTORC1 in comparison to Rapamycin, and induces more cell death in TSC2 null tumors .
    RMC-6272
  • HY-N3239
    Mulberrofuran G

    		NADPH Oxidase HBV
    Mulberrofuran G protects ischemic injury-induced cell death via inhibition of NOX4-mediated ROS generation and ER stress . Mulberrofuran G shows moderate inhibiting activity of hepatitis B virus (HBV) DNA replication with IC50 of 3.99 μM .
    Mulberrofuran G
  • HY-W127530
    α-Tocopherol phosphate disodium
    3 Publications Verification

    alpha-Tocopherol phosphate disodium; TocP disodium; Vitamin E phosphate disodium

    		 Apoptosis Reactive Oxygen Species Cardiovascular Disease
    α-Tocopherol phosphate (alpha-Tocopherol phosphate) disodium, a promising antioxidant, can protect against long-wave UVA1 induced cell death and scavenge UVA1 induced ROS in a skin cell model. α-Tocopherol phosphate disodium possesses therapeutic potential in the inhibition of apoptosis and increases the migratory capacity of endothelial progenitor cells under high-glucose/hypoxic conditions and promotes angiogenesis .
    α-Tocopherol phosphate disodium
  • HY-15588
    L189
    3 Publications Verification

    		 DNA/RNA Synthesis Cancer
    L189 is a DNA ligase inhibitor. L189 has inhibition effect for DNA Ligase I, III and IV with IC50 values of 5 μM, 9 μM and 5 μM, respectively. L189 has no cytotoxicity and individually increase cell death. L189 can be used for the research of cancer .
    L189
  • HY-138215
    ADTL-EI1712

    		ERK Cancer
    ADTL-EI1712 is a potent, orally active, and selective dual-target inhibitor of ERK1 and ERK5, inhibition rates of ERK1/5 at 1 μM are 93.54% and 89.35%, respectively. ADTL-EI1712 can induce regulated cell death, a form of cell death that relies on the activation of genetically encoded machinery, to overcome compensatory mechanism in specific cancer cells in vitro and in vivo .
    ADTL-EI1712
  • HY-114577
    Palifosfamide tromethamine

    Isophosphoramide mustard tromethamine; IPM tromethamine; ZIO-201 tromethamine

    		 DNA Alkylator/Crosslinker Cancer
    Palifosfamide (tromethamine) is a synthetic alkylating agent with potential antineoplastic activity. As the stabilized active metabolite of ifosfamide, palifosfamide (tromethamine) irreversibly alkylates and crosslinks DNA through GC base pairs. This leads to an inhibition of DNA replication and ultimately cell death. Compared to ifosfamide, palifosfamide (tromethamine) is less toxic.
    Palifosfamide tromethamine
  • HY-N6036R
    Ganoderic acid F (Standard)

    		Others Cancer
    Ganoderic acid F (Standard) is the analytical standard of Ganoderic acid F. This product is intended for research and analytical applications. Ganoderic acid F is a ganoderic acid. Ganoderic acid F exhibits antitumor and antimetastatic activities through inhibition of angiogenesis and alteration of proteins involving cell proliferation and/or cell death, carcinogenesis, oxidative stress, calcium signaling, and endoplasmic reticulum stress .
    Ganoderic acid F (Standard)
  • HY-117786
    Go 7874

    		PKC Neurological Disease
    Go 7874 is a protein kinase C (PKC) inhibitor. Go 7874 mediated neuroprotection against LPS/IFNg-induced neuronal cell death in an immune-mediated neurotoxicity model, not through PKC activity. In contrast, the neuroprotective mechanism of Go 7874 involves inhibition of inducible nitric oxide synthase (iNOS) gene expression, followed by reduced nitric oxide (NO) production .
    Go 7874
  • HY-160214
    Perforin-IN-2

    		Others Inflammation/Immunology
    Perforin-IN-2 is a benzosulfonamide perforin inhibitor that alleviates transplant rejection during allogeneic bone marrow/stem cell transplantation. Perforin-IN-2 binds to plasma proteins with a binding rate of 99.8%. Perforin-IN-2 requires a higher concentration (> 900 μM) to achieve optimal perforin inhibition in vivo. Perforin-in-2 can effectively inhibit the lytic activity of recombinant perforin on Jurkat T (IC50=6.65 μM) leukemia cells, and also inhibit the death of K562 leukemia target cells .
    Perforin-IN-2
  • HY-129611
    Bromelain

    		Apoptosis Inflammation/Immunology Cancer
    Bromelain is an anti-inflammatory agent derived from pineapple stem that acts through down-regulation of plasma kininogen, inhibition of Prostaglandin E2 expression, degradation of advanced glycation end product receptors and regulation of angiogenic biomarkers as well as antioxidant action upstream in the COX-pathway . Bromelain exhibits various fibrinolytic, antiedematous, antithrombotic, and anti-inflammatory activities. Bromelain also possesses some anticancerous activities and promotes apoptotic cell death .
    Bromelain
  • HY-147826
    EGFR-IN-60

    		EGFR Apoptosis Cancer
    EGFR-IN-60 (Compound 7d) shows obvious inhibition of EGFR WT, EGFR T790M, EGFR L858R and JAK3 with IC50s of 83, 26, 53, and 69 nM, respectively. EGFR-IN-60 potently inhibits the growth of H1975 cells harboring EGFR T790M mutation (IC50=1.32 µM) over A431 cells overexpressing EGFR WT (IC50=4.96 µM). EGFR-IN-60 exhibits good oral absorption, potent and safe antitumor activity. EGFR-IN-60 induces cell death through apoptosis supported by increased Bax/Bcl-2 ratio .
    EGFR-IN-60
  • HY-117019
    LY150310 free base

    		Others Cancer
    LY150310 is able to inhibit thromboxane synthase, cyclooxygenase, and thrombin activation, biochemical processes that have been proposed in the literature as targets for anti-metastatic agents. The objectives of this study were twofold: (a) to compare the anti-metastatic activity of Eli Lilly compounds with reference anti-metastatic compounds nafazatrom and RA233; and (b) to examine the correlation between inhibition of spontaneous lung metastasis and survival. The anti-metastatic activity of the compounds was evaluated using the Lewis lung squamous cell carcinoma cell model. In this model, 5×10^5 tumor cells were implanted into the gastrocnemius muscle, the primary tumor was resected on day 14, and lung metastatic lesions were counted on day 25. The compounds were administered every 12 hours from day 5 to day 19. Nafazatrom, LY150310, LY189332, and LY135305 were found to inhibit spontaneous lung metastasis in a dose-dependent manner. The ED50 values ??of these compounds were 50, 0.5, 2, and 0.35 mg/kg/day, respectively; the corresponding therapeutic indices (LD50/ED50) were 7, 180, 255, and 511, respectively. To evaluate the effects of nafazatrom, LY150310, LY189332, and LY135305 on animal survival, these compounds were given at the maximum anti-metastatic dose of 200, 60, 20, and 6 mg/kg/day, respectively. Two dosing schedules were used: (a) from day 5 to 19; (b) from day 5 to death. These compounds did not significantly alter median survival times or the number of long-term survivors at any dosing schedule. RA233 did not inhibit lung metastasis or increase median survival time at a schedule in which the maximum tolerated dose of 200 mg/kg/day was given until death on day 5. Postmortem examination of animals given nafazatrom, LY150310, LY189332, and LY1350310 revealed complete suppression of lung lesions, whereas lesions developed in the liver, kidney, spleen, and brain. The results of this study suggest that the effects of a compound on the number of metastatic lesions in target organs may not be predictive of its effects on survival. To successfully translate laboratory data into clinical applications, survival should be considered a predictor of the potential clinical utility of a compound.
    LY150310 free base

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