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PARP cleavage

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86

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1

Inhibitory Antibodies

24

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-10201
    Sorafenib
    Maximum Cited Publications
    283 Publications Verification

    Bay 43-9006

    Raf VEGFR FLT3 Autophagy Apoptosis STAT Akt MMP Cadherin p38 MAPK ERK MEK PI3K PARP Bcl-2 Family Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Sorafenib (Bay 43-9006) is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib inhibits tumor growth and metastasis in mouse and rat models. Sorafenib can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma .
    Sorafenib
  • HY-156498
    RMC-7977
    10+ Cited Publications

    Ras ERK Raf Ribosomal S6 Kinase (RSK) AMPK Apoptosis PARP Cancer
    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 KRAS G12C cancer models, and demonstrates good tolerability across various RAS cancer models .
    RMC-7977
  • HY-10201A
    Sorafenib tosylate
    Maximum Cited Publications
    283 Publications Verification

    Bay 43-9006 tosylate

    Raf VEGFR FLT3 Autophagy Apoptosis STAT Akt MMP Cadherin p38 MAPK ERK MEK PI3K PARP Bcl-2 Family Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma .
    Sorafenib tosylate
  • HY-N0576
    Solanesol
    2 Publications Verification

    Endogenous Metabolite Heme Oxygenase (HO) HSP p38 MAPK Akt Apoptosis Caspase PARP Neurological Disease Metabolic Disease Inflammation/Immunology
    Solanesol is an orally active aliphatic terpene alcohol. Solanesol is mainly found in tobacco and other Solanaceae plants. Solanesol induces HO-1 and Hsp70 expression, activates p38 and Akt signaling pathways, and inhibits Apoptosis (reduces caspase-3 and PARP cleavage). Solanesol has antioxidant, anti-inflammatory, and neuroprotective activities. Solanesol can be used in the research of Huntington's disease, alcoholic liver disease, chronic inflammatory pain, anxiety, Alzheimer's disease, and bipolar disorder .
    Solanesol
  • HY-B1302
    Quinidine hydrochloride monohydrate
    Maximum Cited Publications
    25 Publications Verification

    P-glycoprotein PARP Caspase Apoptosis Potassium Channel Cardiovascular Disease Neurological Disease
    Quinidine hydrochloride monohydrate is an orally active antiarrhythmic agent. Quinidine hydrochloride monohydrate reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride monohydrate exerts sustained block and open-channel block effects on IK(f). Quinidine hydrochloride monohydrate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride monohydrate can be used in studies related to uterine sarcoma and seizures .
    Quinidine hydrochloride monohydrate
  • HY-107545
    Dynole 34-2
    1 Publications Verification

    Dynamin Apoptosis Cancer
    Dynole 34-2 is a potent dynamin GTPase inhibitor (IC50s=6.9 and 14.2 µM for dynamin1 and dynamin2 GTPase activity, respectively) with antimitotic effect. Dynole 34-2 induces apoptosis, as revealed by cell blebbing, DNA fragmentation, and PARP cleavage. Dynole 34-2 also potently inhibits receptor mediated endocytosis (RME) .
    Dynole 34-2
  • HY-P2970

    Apoptosis PARP Caspase Bcl-2 Family Bacterial Interleukin Related Infection Inflammation/Immunology Cancer
    Stem bromelain (EC 3.4.22.32) is a cysteine protease and antibacterial agent. Stem bromelain can be isolated from the stem of the pineapple (Ananas comosus). Stem bromelain induces dose-dependent secretion of IL-12p70, and IL-6, induces Apoptosis, causes cleavage of full-length PARP protein, Caspase 3, and Caspase 9, increases Bax, and decreases Bcl-2. Stem bromelain possesses various fibrinolytic, antiedema, antithrombotic, and anti-inflammatory activities. Stem bromelain also exhibits in vivo antitumor and antileukemic activities, as well as antimetastatic effects. Stem bromelain has antimycobacterial activity. Stem bromelain provides protection against lead poisoning .
    Stem bromelain
  • HY-13326
    ASP3026
    5+ Cited Publications

    Anaplastic lymphoma kinase (ALK) Apoptosis ROS Kinase Caspase PARP IGF-1R STAT Akt JNK Cancer
    ASP3026 is a selective and orally active inhibitor of anaplastic lymphoma kinase (ALK). ASP3026 is a selective and oral active anaplastic lymphoma kinase (ALK) inhibitor with a IC50 value of 3.5 nM. ASP3026 can inhibit the phosphorylation of IGF-1R, STAT3, AKT and JNK proteins, and induce the cleavage of caspase 3 and PARP. It also inhibited ROS and ACK. ASP3026 can be used in anti-tumor research .
    ASP3026
  • HY-125593

    APG-1387

    IAP Apoptosis Cancer
    Dasminapant (APG-1387), a bivalent SMAC mimetic and an IAP antagonist, blocks the activity of IAPs family proteins (XIAP, cIAP-1, cIAP-2, and ML-IAP). Dasminapant induces degradation of cIAP-1 and XIAP proteins, as well as caspase-3 activation and PARP cleavage, which leads to apoptosis. Dasminapant can be used for the research of hepatocellular carcinoma, ovarian cancer, and nasopharyngeal carcinoma .
    Dasminapant
  • HY-171006
    IRF1-IN-1
    1 Publications Verification

    Caspase PARP Pyroptosis Interleukin Related IFNAR Infection Inflammation/Immunology
    IRF1-IN-1 (Compound I-2) is an IRF1 inhibitor. IRF1-IN-1 decreases the recruitment of IRF1 to the promoter of CASP1. IRF1-IN-1 inhibits cell death signaling pathway (i.e., cleavage of Caspase 1, GSDMD, IL-1 and PARP1). IRF1-IN-1 has a protective effect on ionizing radiation-induced inflammatory skin injury .
    IRF1-IN-1
  • HY-138832

    APG-1252-M1

    Bcl-2 Family Apoptosis Caspase PARP Cancer
    BM-1244 (APG-1252-M1) is a Bcl-xL/Bcl-2 inhibitor with Kis of 134 nM and 450 nM. BM-1244 has anti-tumor effects by inducing apoptosis and suppressing tumor growth. BM-1244 can induce cytochrome C and Smac release from mitochondria with caspase-3 and PARP cleavage. BM-1244 exhibits synergy with chemotherapy in vivo. BM-1244 can be studied in research for colorectal cancer, acute myeloid leukemia and gastric cancer .
    BM-1244
  • HY-101985
    BV02
    3 Publications Verification

    Bacterial PARP Caspase Apoptosis Autophagy Akt Infection Neurological Disease Inflammation/Immunology
    BV02 is a 14-3-3 inhibitor and an antibacterial agent. BV02 enhances the cleavage of PARP and caspase-3. BV02 induces Apoptosis, Autophagy, and enhances Akt activation. BV02 has anti-B. melitensis infection and epilepsy-promoting effects. BV02 can also be used in colitis research.
    BV02
  • HY-N11908

    cis-α-Santalol

    Akt Survivin Apoptosis Caspase PARP Metabolic Disease Cancer
    α-Santalol (cis-α-Santalol), a naturally occurring sesquiterpene, is an orally active anticancer agent and apoptosis inducer. α-Santalol activates caspase-3 to drive apoptotic processes. >α-Santalol induces apoptosis, decreases cell viability, and causes PARP cleavage in human prostate cancer cells. α-santalol inhibits Akt/Survivin pathway to induce cell death. α-Santalol can be used for the research of prostate cancer and diabetes mellitus .
    α-Santalol
  • HY-153188

    PROTACs Apoptosis IRAK Cancer
    JNJ-1013 is a potent and selective IRAK1 PROTAC degrader with an IC50s of 72, 443, 1071 nM for IRAK1, IRAK4, VHL FP respectively. JNJ-1013 induces apoptosis and increases the expression of cleavaged PARP. JNJ-1013 decreases the expression IRAK1, p-IKBα, pSTAT3(Tyr705) (Pink: ligand for target protein (HY-138834); black: linker (HY-Y1760); Blue: E3 ligase ligand (HY-112078)) .
    JNJ-1013
  • HY-N2993

    Apoptosis Caspase PARP Akt PTEN MDM-2/p53 JNK Cancer
    Polyporenic acid C is a lanostane-type triterpenoid. Polyporenic acid C can be isolated from Poria cocos. Polyporenic acid C causes the cleavage of caspase-8 and caspase-3, as well as the cleavage of PARP. Polyporenic acid C reduces the phosphorylation level of Akt (Ser473), increases the phosphorylation of PTEN and p53 (Ser15), and activates JNK. Polyporenic acid C induces Apoptosis. Polyporenic acid C shows anticancer activity against non-small cell lung cancer .
    Polyporenic acid C
  • HY-N3126

    Drug Derivative Fungal Apoptosis Caspase PARP Neurological Disease Cancer
    Orsellinic acid is a Benzoic acid (HY-N0216) derivative. Orsellinic acid can be isolated from Chaetomium globosum endophytic on Ephedra fasciculata (Mormon tea). Orsellinic acid blocks PAF-mediated Apoptosis, inhibits caspase-3/7 activation, and PARP cleavage. Orsellinic acid can be used in research of neurons and various tumors (non-small cell lung cancer, breast cancer, neuroblastoma, pancreatic cancer) .
    Orsellinic acid
  • HY-171007
    IRF1-IN-2
    1 Publications Verification

    Caspase PARP Pyroptosis Interleukin Related Glutathione Peroxidase IFNAR Infection Inflammation/Immunology
    IRF1-IN-2 (Compound I-19) is an IRF1 inhibitor. IRF1-IN-2 decreases the recruitment of IRF1 to the promoter of CASP1. IRF1-IN-2 inhibits cell death signaling pathway (i.e., cleavage of Caspase 1, GSDMD, IL-1 and PARP1; inhibits the Pho of TKB1, upregulates GPX4 and downregulates FACL4). IRF1-IN-2 has a protective effect on ionizing radiation-induced inflammatory skin injury .
    IRF1-IN-2
  • HY-N2132
    Flavokawain B
    2 Publications Verification

    Flavokavain B

    Apoptosis Caspase PARP Bcl-2 Family NF-κB PI3K Akt p38 MAPK MMP Reactive Oxygen Species (ROS) Cardiovascular Disease Inflammation/Immunology Cancer
    Flavokawain B (Flavokavain B) is an orally active chalcone. Flavokawain B results in activation of caspase-9, -3 and -8, cleavage of PARP. Flavokawain B down-regulates Bcl-2 with concomitant increase in Bax level. Flavokawain B inhibits NF-κB, PI3K/Akt and MAPK signaling pathway. Flavokawain B exhibits Apoptotic effects. Flavokawain B inhibits MMP-9 and promotes ROS generation. Flavokawain B inhibits multiple tumors and inflammation .
    Flavokawain B
  • HY-N2445
    Flavokawain C
    4 Publications Verification

    Apoptosis Akt JNK PERK Caspase PARP MDM-2/p53 IAP Reactive Oxygen Species (ROS) SOD FABP Autophagy AMPK mTOR GLUT EGFR PI3K HSP VEGFR FAK Cancer
    Flavokawain C is an orally active natural chalcone. Flavokawain C inhibits the proliferation of various cancer cells. Flavokawain C upregulates GADD153 in cancer cells, inhibits the phosphorylation of Akt and JNK, suppresses early ERK phosphorylation, activates late ERK phosphorylation, activates caspase related subtypes, induces PARP-1 cleavage, causes upregulation of p21 and p27, downregulation of mutant p53 and anti-apoptotic IAP proteins, elevates intracellular ROS levels, reduces SOD activity, and induces apoptosis. Flavokawain C downregulates FABP4, induces autophagy in cancer cells, and activates the AMPK/mTOR pathway . Flavokawain C decreases the expression of glycolysis-related proteins GLUT1 and HK2, and inhibits glycolysis in nasopharyngeal carcinoma cells. Flavokawain C inhibits the activation of the EGFR/PI3K/Akt/mTOR signaling pathway and reduces the expression of HSP90B1. Flavokawain C inhibits angiogenesis by decreasing the expression of angiogenic proteins Ang-1 and VEGF in human umbilical vein endothelial cells. Flavokawain C increases γ-H2AX levels in cells, inhibits the phosphorylation of FAK, PI3K and AKT in cells, and induces DNA damage in cells. Flavokawain C exerts anti-tumor activity in multiple tumor xenograft mouse models. Flavokawain C is applicable to research related to colorectal cancer, colon adenocarcinoma, nephroblastoma, nasopharyngeal carcinoma and liver cancer .
    Flavokawain C
  • HY-114324

    PROTACs PARP Cancer
    PROTAC PARP1 degrader is a PARP1 degrader based on MDM2 E3 ligand. PROTAC PARP1 degrader induces significant PARP1 cleavage and programmed cell death. PROTAC PARP1 degrader consists of E3 ubiquitinase ligand MDM2 ligand (HY-128836), blue part; target protein ligand PAPR1 ligand (HY-171543), pink part; PROTAC linker N3-PEG4-C2-NH2 (HY-128834), black part .
    PROTAC PARP1 degrader
  • HY-W028690
    DNMDP
    4 Publications Verification

    Phosphodiesterase (PDE) Cancer
    DNMDP, a phosphodiesterase 3A (PDE3A) inhibitor, is a potent and selective cancer cell cytotoxic agent. DNMDP binding to PDE3A promotes an interaction between PDE3A and Schlafen 12 (SLFN12). DNMDP shows clear cell-selective cytotoxicity .
    DNMDP
  • HY-147291

    c-Myc PARP Apoptosis Cancer
    VPC-70063 is a potent Myc-Max inhibitor with an IC50 value of 8.9 μM for Myc-Max transcriptional activity inhibition. VPC-70063 reduces UBE2C promotor activity and AR-V7 levels, and induces PARP cleavage. VPC-70063 induces apoptosis and blocks Myc-Max interactions with DNA. VPC-70063 can be used for researching anticancer .
    VPC-70063
  • HY-111329
    JGB1741
    1 Publications Verification

    ILS-JGB-1741

    Sirtuin Apoptosis Cancer
    JGB1741 (ILS-JGB-1741) is a potent and specific SIRT1 activity inhibitor with an IC50 of ∼15 μM. JGB1741 is a weak SIRT2 and SIRT3 inhibitor with an all IC50>100 μM. JGB1741 increases the acetylated p53 levels leading to p53-mediated apoptosis with modulation of Bax/Bcl2 ratio, cytochrome c release and PARP cleavage. JGB1741 has the potential for breast cancer research .
    JGB1741
  • HY-128153
    Thienopyridone
    1 Publications Verification

    Phosphatase Apoptosis Cancer
    Thienopyridone is a potent and selective phosphatase of regenerating liver (PRL) phosphatase inhibitor with IC50s of 173 nM, 277 nM and 128 nM for PRL-1, PRL-2, and PRL-3, respectively. Thienopyridone shows minimal effects on other phosphatases. Thienopyridone induces p130Cas cleavage and apoptosis and has anticancer effects .
    Thienopyridone
  • HY-N6861

    Apoptosis Cancer
    Lucidenic acid B is a natural compound isolated from Ganoderma lucidum, induces apoptosis of cancer cells, and causes the activation of caspase-9 and caspase-3, and cleavage of PARP. Lucidenic acid B does not affect the cell cycle profile, or the number of necrotic cells .
    Lucidenic acid B
  • HY-114324A

    PROTACs PARP Cancer
    rel-PROTAC PARP1 degrader is the relative configuration of ROTAC PARP1 degrader (HY-114324). ROTAC PARP1 degrader is a PARP1 degrader based on MDM2 E3 ligand. It induces significant PARP1 cleavage and programmed cell death. PROTAC PARP1 degrader at 10 μM at 24 h inhibits MDA-MB-231 cell line with an IC50 of 6.12 μM.
    rel-PROTAC PARP1 degrader
  • HY-W748509

    Caspase Apoptosis Cancer
    Pipernonaline is a piperine derivative with antiprostate cancer activity. Pipernonaline inhibits the proliferation of androgen-dependent/independent LNCaP/PC-3 prostate cells. Pipernonaline activates caspase-3 and promotes procaspase-3/PARP cleavage. Pipernonaline also mediates reactive oxygen species (ROS) production, increased intracellular Ca(2+), and mitochondrial membrane depolarization .
    Pipernonaline
  • HY-131688

    PARP Caspase Inflammation/Immunology
    2-Chlorohexadecanoic acid, an inflammatory lipid mediator, interferes with protein palmitoylation,induces ER-stress markers, reduced the ER ATP content, and activates transcription and secretion of IL-6 as well as IL-8.2-Chlorohexadecanoic acid disrupts the mitochondrial membrane potential and induces procaspase-3 and PARP cleavage.2-Chlorohexadecanoic acid can across blood-brain barrier (BBB) and compromises ER- and mitochondrial functions in the human brain endothelial cell line hCMEC/D3 .
    2-Chlorohexadecanoic acid
  • HY-N16483

    Apoptosis Caspase Bcl-2 Family PARP Androgen Receptor Cancer
    Procyanidin B2-3'-O-gallate is a mono-gallate ester that can be isolated from grape seed extract. Procyanidin B2-3'-O-gallate has anti-cancer efficacy and reduces the viability of prostate carcinoma LNCaP cells. Furthermore, Procyanidin B2-3'-O-gallate induces apoptosis, and causes caspases-9 and -3 and PARP cleavage, and down-regulates Bcl-2, Bcl-Xl and androgen receptor levels .
    Procyanidin B2-3'-O-gallate
  • HY-N12999

    Apoptosis Bcl-2 Family Caspase MDM-2/p53 PARP Amylases Metabolic Disease Endocrinology Cancer
    Stigmast-5-en-3-ol induces cancer cell apoptosis and inhibits proliferation by increasing the production of Bax, Caspase-9, p53, and PARP cleavage and reducing Bcl-xl expression. Stigmast-5-en-3-ol exhibits potent inhibitory activity against glucoamylase and α-amylase and possesses high antioxidant activity. Stigmast-5-en-3-ol can be used in the research of diseases such as leukemia, breast cancer, type 2 diabetes, and obesity .
    Stigmast-5-en-3-ol
  • HY-N6576

    p38 MAPK ERK JNK IAP PARP Apoptosis Caspase Cancer
    Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers .
    Hellebrigenin
  • HY-150696

    Apoptosis Caspase PARP Cancer
    Antitumor agent-72 (compound 6w) is a potent anticancer agent. Antitumor agent-72 has anticancer activity and induces apoptosis through activation of caspase-3 and cleavage of PARP. Antitumor agent-72 can be used for cancer research .
    Antitumor agent-72
  • HY-101597

    Apoptosis Cancer
    NVX-207, a Betulinic acid-derived anti-cancer compound, shows anti-tumor activity (mean IC50=3.5 μM) against various human and canine cell lines. NVX-207-induced apoptosis is associated with activation of the intrinsic apoptotic pathway via cleavage of caspases -9, -3, -7 and of PARP .
    NVX-207
  • HY-178749

    ClpP Mitochondrial Metabolism Apoptosis Caspase PARP Cancer
    MS6076 is a mitochondrial protease ClpP agonist. MS6076 specifically activates the ClpP protease in the mitochondrial matrix, significantly disrupting mitochondrial Electron Transport Chain (ETC) function by accelerating the degradation of unfolded proteins. MS6076 exhibits potent cytotoxicity against a variety of cancer cell lines. MS6076 induces cell apoptosis, increasing cleavage of caspase 3 and PARP. MS6076 can be used for the research of breast cancer .
    MS6076
  • HY-124791

    MDM-2/p53 PARP Cancer
    MMRi6 is a Mdm2-MdmX RING domain inhibitor that can disrupt Mdm2-MdmX RING-RING interaction in vitro. MMRi6 inhibits MdmX-stimulated Mdm2 autoubiquitination and Mdm2-MdmX-mediated p53 polyubiquitination in vitro without affecting NEDD4-1 autoubiquitination. MMRi6 induces p53 stabilization and accumulation and induces PARP cleavage in wt-p53 Emu-myc lymphoma cells. MMRi6 inhibits the growth of wt-p53 and p53-null Emu-myc lymphoma cells with IC50s of approximately 0.5 μM and 3 μM, respectively. MMRi6 can be used for the study of leukemia/lymphoma .
    MMRi6
  • HY-N7569

    Apoptosis Caspase PPAR Cancer
    Demethoxyfumitremorgin C is a secondary metabolite of the marine fungus, Aspergillus fumigatus. Demethoxyfumitremorgin C induces prostate cancer cell apoptosis. Demethoxyfumitremorgin C activates caspase-3, -8, and -9, leading to PARP/ cleavage .
    Demethoxyfumitremorgin C
  • HY-178178

    PARP Reactive Oxygen Species (ROS) DNA/RNA Synthesis Apoptosis Cancer
    PARP1-IN-46 is a potent PARP-1 inhibitor with an IC50 of 2.4 nM. PARP1-IN-46 demonstrates remarkable anti-proliferative activity in both rat (C6) and human (U87MG) glioma cells. PARP1-IN-46 promotes PARP cleavage, triggers DNA damage, and increases ROS. PARP1-IN-46 effectively inhibits the migration, invasion and colony formation of glioma cells, and ultimately induces cell apoptosis. PARP1-IN-46 can be used to the study of glioma .
    PARP1-IN-46
  • HY-178099

    Apoptosis Caspase PARP Bcl-2 Family Cancer
    Apoptosis inducer 45 is an apoptosis inducer. Apoptosis inducer 45 is cytotoxically active against the MCF-7 cell line. Apoptosis inducer 45 elicits MCF-7 cell apoptosis via the mitochondrial pathway (increases the Bax/Bcl-2 ratio) by activating cleavage of caspase-9, thereby inducing the fragmentation of DNA repair protein PARP. Apoptosis inducer 45 also can induce caspase-8 cleavage, subsequently initiating cleavage of caspase-3 and its downstream protein PARP to culminate in the extrinsic apoptosis. Apoptosis inducer 45 can be used in the research of breast cancer .
    Apoptosis inducer 45
  • HY-146096

    P-glycoprotein Apoptosis Cancer
    RMS3, a tetrandrine analogue, is a potent P-glycoprotein (P-gp) inhibitor. RMS3 has markedly antiproliferative and cytotoxic effects on cancer cells. RMS3 causes PARP cleavage, a marker for cells undergoing apoptosis. RMS3 has strong anticancer property .
    RMS3
  • HY-171184

    PARP Bcr-Abl Apoptosis Mitosis Cancer
    EAPB0503 is a quinoline compound with anti-tumor activity, showing strong cytotoxicity against melanoma cells in vitro (IC50=200 nM). EAPB0503 can induce specific cell cycle arrest in mitosis of CML cells and directly activate apoptosis, leading to an increase in the G0 cell population, disruption of mitochondrial membrane potential, PARP cleavage, and DNA fragmentation. EAPB0503 also reduces the levels of BCR-ABL protein .
    EAPB0503
  • HY-178116

    EGFR PARP Cancer
    HER2-IN-23 is a selective HER2 inhibitor. HER2-IN-23 reduces in total HER2 expression rather than in phosphorylated HER2 (p-HER2). HER2-IN-23 reduces cyclin D1 level and stimulates PARP cleavage. HER2-IN-23 can be used for the study of HER2-positive breast cancer .
    HER2-IN-23
  • HY-170995

    PROTACs ROR Apoptosis Cancer
    PROTAC ROR1 degrader-1 (Compound 11d) is a PROTAC degrader for pseudokinase ROR1 that degrades ROR1 in NSCLC cells with a DC50s of 40-80 nM. PROTAC ROR1 degrader-1 causes the cleavage of PARP and induces apoptosis in NCI-H23 . (Pink: ligand for target protein ROR1 ligand-1 (HY-170996); Black: linker (HY-W014787); Blue: ligand for VHL E3 ligase (S,R,S)-AHPC (HY-125845))
    PROTAC ROR1 degrader-1
  • HY-118522

    Proteasome NF-κB Caspase PARP IAP Apoptosis Cancer
    TP-110 is a proteasome inhibitor. TP-110 specifically inhibits the protease-like activity of the 20S proteasome, but does not affect the trypsin-like or peptidyl-glutamyl peptide hydrolysis activity. TP-110 inhibits the NF-κB pathway, activates caspase-8, -9, and -3, and causes PARP cleavage, significantly reducing the levels of cIAP-1 and XIAP. TP-110 causes cell cycle arrest at the G2/M phase and promotes apoptosis of cancer cells. TP-110 can be used in cancer research of prostate cancer and multiple myeloma, etc .
    TP-110
  • HY-N0576R

    Reference Standards Endogenous Metabolite Heme Oxygenase (HO) HSP p38 MAPK Akt Apoptosis Caspase PARP Neurological Disease Metabolic Disease Inflammation/Immunology
    Solanesol (Standard) is the analytical standard of Solanesol (HY-N0576). This product is intended for research and analytical applications. Solanesol is an orally active aliphatic terpene alcohol. Solanesol is mainly found in tobacco and other Solanaceae plants. Solanesol induces HO-1 and Hsp70 expression, activates p38 and Akt signaling pathways, and inhibits Apoptosis (reduces caspase-3 and PARP cleavage). Solanesol has antioxidant, anti-inflammatory, and neuroprotective activities. Solanesol can be used in the research of Huntington's disease, alcoholic liver disease, chronic inflammatory pain, anxiety, Alzheimer's disease, and bipolar disorder .
    Solanesol (Standard)
  • HY-174302

    Pim HDAC PARP Apoptosis Cancer
    PIM-1/HDAC-IN-2 is a robust PIM/HDAC inhibitor (IC50 = 0.11 μM in MV4-11cells), which exerts a synergistic antiproliferative effect through a dual mechanism of inhibiting PIM1 kinase and selectively inhibiting HDAC6. PIM-1/HDAC-IN-2 induces cell apoptosis. PIM-1/HDAC-IN-2 remarkably induces the cleavage of PARP, thereby initiating the arrest of the cell cycle in G1 phase and a reduction in S phase. PIM-1/HDAC-IN-2 demonstrates significant anticancer efficacyin the MV4-11 xenograft model without notable toxicity[1].
    PIM-1/HDAC-IN-2
  • HY-178351

    HDAC Microtubule/Tubulin Apoptosis Caspase Bcl-2 Family Cancer
    HDAC6-IN-67 is a selective HDAC6 inhibitor (IC50 = 17.15 nM) that exhibits 19-fold selectivity over HDAC1. HDAC6-IN-67 selectively inhibits HDAC6 by interacting with Ser531 and His614. HDAC6-IN-67 induces apoptosis by inducing the cleavage of caspases 9, 8, 3, and PARP, upregulating Bax expression, and downregulating Bcl-2 expression. HDAC6-IN-67 effectively induces the acetylation of α-tubulin, without affecting histone H3 acetylation in MCF-7/ADR cells. HDAC6-IN-67 can be used for the study of breast cancer .
    HDAC6-IN-67
  • HY-120339

    Microtubule/Tubulin FAK MEK ERK MMP Caspase PARP Apoptosis MDM-2/p53 Cancer
    STK899704 is a tubulin polymerization inhibitor. STK899704 exhibits broad-spectrum inhibitory activity against various cancer cell lines with IC50 values ​​ranging from 0.2 to 1.0 μM. STK899704 disrupts the mitotic spindle structure, inducing G2/M phase cell cycle arrest. STK899704 inhibits the migration ability of HT29 cells by downregulating the FAK-MEK-ERK signaling pathway, thereby suppressing the expression and activity of MMP-2 and MMP-9. STK899704 activates caspase-3/7/8/9, leading to PARP cleavage and inducing apoptosis. STK899704 induces cellular senescence through the p53 pathway. STK899704 can be used in research on skin cancer, lung cancer, colon cancer, and other cancers .
    STK899704
  • HY-149017

    Apoptosis Cancer
    Apoptosis inducer 7 (Compound 5I) induces apoptosis in cancer cells. Apoptosis inducer 7 inducrs cleavage of PARP, caspases, down-regulation of anti-apoptotic protein c-Flip and up regulation of pro-apoptotic protein Noxa. Apoptosis inducer 7 exhibits antitumor activity .
    Apoptosis inducer 7
  • HY-17548

    Caspase Apoptosis Cancer
    VMY-1-103 is an inhibitor for cyclin/Cdk complex, that arrests the cell cycle at G1 phase. VMY-1-103 reduces mitochondrial membrane potential, induces p53 phosphorylation and and PARP cleavage, activates caspase-3, and thus induces apoptosis in prostate cancer cell LNCaP .
    VMY-1-103
  • HY-147514

    Apoptosis Caspase PARP Bcl-2 Family Cancer
    Anticancer agent 64 (compound 5m) shows cytotoxic activity in CCRF-CEM cells, with IC50 of 2.4 μM. Anticancer agent 64 shows good anticancer activity through apoptosis induction. Anticancer agent 64 induces caspase 3 and 7 activation and PARP cleavage. Anticancer agent 64 induces significant effect of mitochondria depolarization .
    Anticancer agent 64

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