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NAD depletion

" in MedChemExpress (MCE) Product Catalog:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-50876
    Daporinad
    Maximum Cited Publications
    64 Publications Verification

    FK866; APO866

    		 NAMPT Autophagy Apoptosis mTOR p38 MAPK ERK Cancer
    Daporinad (FK866) is a non-competitive inhibitor of nicotinamide phosphoribosyltransferase (Nampt), with a Ki value of 0.3 nM. Daporinad depletes NAD+ and ATP levels, inhibits mTORC1 and MAPK/ERK pathways, and activates TFEB to induce autophagy. Daporinad causes the depletion of the endoplasmic reticulum Ca²⁺ pool, ultimately weakening the mitogen-induced Ca²⁺ signal and the activation and function of T cells. Daporinad induces cell cycle arrest and apoptosis, and inhibits cell proliferation. Daporinad can be used for the study of myeloma, liver cancer, and immunosuppression .
    Daporinad
  • HY-W614507
    Dihydronicotinamide riboside

    		NADPH Oxidase Apoptosis Bcl-2 Family Metabolic Disease Cancer
    Dihydronicotinamide riboside is a potent NAD + concentration enhancer. Dihydronicotinamide riboside modulates targets BAX, PUMA, NQO2, and IκB kinase. Dihydronicotinamide riboside mediates apoptosis, induces pro-oxidant activity, mitochondrial dysfunction, metabolic dysregulation, redox modulation, and pro-inflammatory M1 phenotype induction. Dihydronicotinamide riboside increases intracellular and mitochondrial NAD + levels, maintains cell survival against NAD +-depleting genotoxins. Dihydronicotinamide riboside can be used for the research of hepatocellular carcinoma .
    Dihydronicotinamide riboside
  • HY-178159
    SA91-0178

    		RNA MTase Inflammation/Immunology
    SA91-0178 is a METTL1 inhibitor. SA91-0178 inhibits m 7G methylation of RNA, reduces SARM1 stability, mitigates NAD + depletion and metabolic reprogramming in macrophages. SA91-0178 demonstrates excellent protective efficacy against multiple organ injury in cecal ligation and puncture (CLP)-induced and ischemia/reperfusion (I/R)-induced mice. SA91-0178 can be used for the study of systemic inflammatory diseases .
    SA91-0178
  • HY-12628
    GNE-618
    2 Publications Verification

    		 NAMPT Cancer
    GNE-618 is a potent, orally active nicotinamide phosphoribosyl transferase (NAMPT) inhibitor with an IC50 of 6 nM. GNE-618 depletes NAD levels and induces tumor cell death. Anti-tumor activity .
    GNE-618
  • HY-173679
    RBN012811

    		PROTACs PARP Interleukin Related STAT Integrin HSV VSV Infection Cancer
    RBN012811 is a highly selective PROTAC-based PARP14 degrader. RBN012811 forms a ternary complex with cereblon by binding to the NAD + site of PARP14, and mediates the specific degradation of PARP14 via the ubiquitin-proteasome pathway (IC50=10 nM). RBN012811 effectively depletes endogenous PARP14 in various cell lines and primary human macrophages, thereby downregulating IL-10 production and IFN-β mRNA levels, increasing phosphorylated STAT1 levels to enhance inflammatory signaling, and inhibiting interferon-induced ADPr condensate formation. RBN012811 also modulates viral replication, exhibiting increased HSV1 replication while reducing VSV replication. RBN012811 has important application value in research related to cancer and viral infections .
    RBN012811
  • HY-14374
    GPP78

    CAY10618

    		 NAMPT Autophagy Inflammation/Immunology Cancer
    GPP78 (CAY10618) is a potent Nampt inhibitor with an IC50 of 3.0 nM for nicotinamide adenine dinucleotide (NAD) depletion. GPP78 is cytotoxic to neuroblastoma cell line SH-SY5Y cells with an IC50 of 3.8 nM by inducing autophagy. GPP78 has anti-cancer and anti-inflammatory effects .
    GPP78
  • HY-125147
    A-1293201

    		NAMPT Cancer
    A-1293201 is a substrate-independent NAMPT inhibitor with antitumor activity. A-1293201 effectively reduces the total cellular NAD +/NADH (NADt) level, subsequently leading to ATP depletion and cancer cell death. In addition, A-1293201 can effectively overcome the acquired resistance mechanism of the NAMPT Y18 mutant to CHS-828 (HY-10079) .
    A-1293201
  • HY-110319
    (E/Z)-Daporinad hydrochloride

    (E/Z)-FK866 hydrochloride; (E/Z)-APO866 hydrochloride

    		 NAMPT Apoptosis Inflammation/Immunology Cancer
    (E/Z)-Daporinad hydrochloride ((E/Z)-FK866 hydrochloride) is a potent inhibitor of nicotinamide phosphoribose transferase (NAMPT). (E/Z)-Daporinad hydrochloride induces apoptosis by specifically inhibiting NAMPT to gradually deplete intracellular NAD +. (E/Z)-Daporinad hydrochloride can be used in the study of cancer biology and inflammatory diseases .
    (E/Z)-Daporinad hydrochloride
  • HY-50876A
    Daporinad hydrochloride

    FK866 hydrochloride; APO866 hydrochloride

    		 NAMPT Autophagy Apoptosis mTOR p38 MAPK ERK Inflammation/Immunology Cancer
    Daporinad (FK866) hydrochloride is a non-competitive inhibitor of nicotinamide phosphoribosyltransferase (Nampt), with a Ki value of 0.3 nM. Daporinad hydrochloride depletes NAD+ and ATP levels, inhibits mTORC1 and MAPK/ERK pathways, and activates TFEB to induce autophagy. Daporinad hydrochloride causes the depletion of the endoplasmic reticulum Ca²⁺ pool, ultimately weakening the mitogen-induced Ca²⁺ signal and the activation and function of T cells. Daporinad hydrochloride induces cell cycle arrest and apoptosis, and inhibits cell proliferation. Daporinad hydrochloride can be used for the study of myeloma, liver cancer, and immunosuppression .
    Daporinad hydrochloride
  • HY-181578
    Nampt-IN-17

    		NAMPT Apoptosis Cancer
    Nampt-IN-17 is an selective orally active NAMPT inhibitor with a human NAMPT IC50 of 17 nM and Ki of 25.9 nM. Nampt-IN-17 depletes intracellular NAD + and ATP, disrupts mitochondrial membrane potential, suppresses cell proliferation, self-renewal, invasion, and migration, induces cell-cycle arrest and apoptosis. Nampt-IN-17 exhibits selective activity against NAPRT-deficient gastric cancer cells. Nampt-IN-17 can be used for the research of NAPRT-deficient gastric cancer .
    Nampt-IN-17

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