parp cleavage

Rubiadin (1,3-Dihydroxy-2-Methylanthracene-9,10-Dione) possesses potent antioxidant property, it can prevent lipid peroxidation induced by FeSO4 and t-butylhydroperoxide (t-BHP) in a dose dependent manner.

JGB1741 (ILS-JGB-1741) is a potent and selective inhibitor of SIRT1 with an IC50 of 15 μM. It modulates the Bax/Bcl2 ratio, cytochrome c release, and PARP cleavage, and increases acetylated p53 levels, leading to p53-mediated apoptosis. JGB1741 can be used in breast cancer studies.

MDK83190 (Apoptosis Activator 2) is a potent apoptosis activator, induceing caspase-3 activation, PARP cleavage, and DNA fragmentation .

PROTACROR1degrader-1 (Compound 11d) serves as a PROTAC degrader targeting the pseudokinase ROR1, with the capability of degrading ROR1 in NSCLC cells at a DC50 of 40-80 nM. It induces PARP cleavage and apoptosis in NCI-H23 cells. [Pink: ligand for target protein ROR1 ligand-1; Black: linker; Blue: ligand for VHL E3 ligase (S,R,S)-AHPC]

Anticanceragent 201 (Compound 2f) exhibits IC50 values in the low micromolar range across various tumor cell lines. It demonstrates high in vitro cytotoxicity against CCRF-CEM cells by inducing apoptosis through the activation of caspase-3 in the mitochondrial intrinsic pathway, cleavage of PARP, and reduced expression of Bcl-2 and Bcl-XL proteins. Anticanceragent 201 can be utilized in cancer research.

PIM-1/HDAC-IN-2 is a potent dual inhibitor of PIM/HDAC, exhibiting an IC50 value of 0.11 μM. It synergistically impedes cell proliferation through the inhibition of PIM1 kinase and the selective suppression of HDAC6. This compound effectively induces PARP cleavage, causing cell cycle arrest in the G1 phase and reducing S phase cells. PIM-1/HDAC-IN-2 demonstrates significant anticancer activity in the MV4-11 tumor xenograft model, with minimal toxicity.

MMRi6 is an inhibitor of the Mdm2-MdmX RING domain, capable of disrupting Mdm2-MdmX RING-RING interactions in vitro. It inhibits MdmX-stimulated Mdm2 autoubiquitination and Mdm2-MdmX-mediated polyubiquitination of p53 without affecting NEDD4-1 autoubiquitination. In wt-p53 Emu-myc lymphoma cells, MMRi6 induces p53 stabilization and accumulation, as well as PARP cleavage. It inhibits the growth of wt-p53 and p53-null Emu-myc lymphoma cells, with IC50 values of approximately 0.5 μM and 3 μM, respectively. MMRi6 is applicable in leukemia/lymphoma research.

Erucin （1-isothiocyanato-4-methylsulfanylbutane） is a dietary isothiocyanate produced by enzymatic hydrolysis of glucoErucin with potential cancer preventive effects, involved in apoptosis and cell cycle blockade through PARP-1 cleavage, p53 and p21，Cyp450, quinone reductase (QR), glutatione transferase (GST) and other pathways.

MPT0B206 is a novel tubulin polymerization inhibitor. MPT0B206 induced G2/M cell cycle arrest and the appearance of the mitotic marker MPM-2 in K562 and K562R cells, which is associated with the upregulation of cyclin B1 and the dephosphorylation of Cdc2.

NiCur is an effective and selective inhibitor of CBP histone acetyltransferase (HAT), with an IC50 of 0.35 μM. NiCur blocks CBP HAT activity, downregulates p53 activation and inhibits apoptosis, while promoting methylation of Lysine 27 on histone H3, inhibiting Caspase 3 activity and PARP cleavage.

Antitumor agent-72 (compound 6w) is a potent anticancer agent that induces apoptosis by activating caspase-3 and cleaving PARP, making it valuable for cancer research [1].

Anticancer agent 64 (compound 5m) exhibits potent cytotoxicity against CCRF-CEM cells with an IC50 value of 2.4 μM, induces apoptosis by activating caspase 3 and 7 and causing PARP cleavage, and significantly disrupts mitochondrial membrane potential, thereby contributing to its anticancer efficacy [1].

RMS5 is a hambanine analogue and a potent P-glycoprotein (P-gp) inhibitor.RMS5 has significant anti-proliferative and cytotoxic effects on cancer cells.RMS5 slightly reduces the expression of the anti-apoptotic Bcl-2 family proteins Bcl-XL and Mcl-1.RMS3 causes cleavage of PARP, a marker of apoptosis.RMS5 has strong anti-cancer properties. RMS5 has strong anti-cancer properties.

WP-1034 is a novel Jak-Stat inhibitor, which is active against AML blasts. WP-1034 effectively inhibited proliferation of OCIM2 cells and fresh AML samples. WP-1034 caused cell cycle arrest of OCIM2 cells in sub-Go phase. WP-1034 induced apoptosis of OCIM2 cells and that induction of apoptosis involved cleavage of caspase 3 and the DNA repair enzyme poly (adenosine diphosphate [ADP]-ribose) polymerase (PARP).

L-Chicoric Acid (trans-Caffeoyltartaric acid) has been shown to inhibit hyaluronidase and HIV-1 integrase, and to possess phagoeytosis stimulatory activity in vitro and in vivo and antiviral acitivy. L-Chicoric acid may reduce acute alcohol-induced steatosis in mice through interfering with the induction of iNOS and iNOS-dependent signaling cascades in the liver. 3. L-Chicoric acid inhibited cell viability and induced apoptosis in 3T3-L1 preadipocytes which was characterized by chromatin condensation and poly ADP-ribose-polymerase (PARP) cleavage.

DAT-230 is a promising microtubule inhibitor that has great potential for the treatment of fibrosarcoma in vitro and in vivo. DAT-230 exhibited potent anti-proliferative activity against various cancer cells. DAT-230 -treatment in HT-1080 cells resulted in microtubule de-polymerization and G2/M phase arrest preceding apoptosis. Phosphor-cdc2 (thr14/tyr15) reduction, cyclin B1 accumulation and aberrant spindles denoted the cyclin B1-cdc2 complex active and M phase arrest in HT-1080 cells treated with DAT-230. Apoptosis induced by DAT-230 was related with the activation of caspase-9, caspase-3 and PARP cleavage, which were at the downstream of mitochondria.

APX2014 is a novel potent and specific Ref-1 inhibitor, blocking in vitro cell proliferation and activating apoptosis via PARP cleavage.

VMY-1-103 is a potent CDK inhibitor, is also a novel dansylated analog of purvalanol B, was shown to inhibit cell cycle progression and proliferation in prostate and breast cancer cells more effectively than purvalanol B. VMY-1-103 , but not purvalanol B, significantly decreased the proportion of cells in S phase and increased the proportion of cells in G(2)/M. VMY-1-103 increased the sub G(1) fraction of apoptotic cells, induced PARP and caspase-3 cleavage and increased the levels of the Death Receptors DR4 and DR5, Bax and Bad while decreasing the number of viable cells, all supporting apoptosis as a mechanism of cell death. VMY-1-103 possesses unique antiproliferative capabilities and that this compound may form the basis of a new candidate drug to treat medulloblastoma.

Compound A5b, also known as JMJD3/HDAC-IN-1, is a dual inhibitor that targets both JMJD3 (Jumonji domain-containing protein demethylase 3) and HADC1 (histone deacetylase, IC50 = 16 nM). It induces hypermethylation of histone H3K27 and hyperacetylation of H3K9, while also promoting apoptosis through the cleavage of caspase-7 and PARP. This compound has demonstrated the ability to effectively inhibit cancer cell cloning, migration, and invasion [1].

BET-IN-20 (compound 10), a BRD4 BD1 inhibitor (IC 50 =1.9 nM), exhibits significant anticancer properties. It promotes apoptosis in acute myeloid leukemia (AML) cells and arrests the cell cycle in the G0/G1 phase. Additionally, BET-IN-20 inhibits both c-Myc and CDK6, and enhances PARP cleavage [1].

PAWI-2 functions as both a p53 activator and a Wnt inhibitor. It suppresses β3-KRAS signaling independently of KRAS and selectively inhibits the phosphorylation of TBK1. Additionally, PAWI-2 triggers apoptosis (activation of caspase-3/7) and induces PARP cleavage. It facilitates the translocation of retinoblastoma protein into the nucleus, leading to G2/M cell cycle arrest. PAWI-2 reverses the cancer stem cell-like properties of KRAS-dependent human pancreatic cancer stem cells (hPCSC) and overcomes drug resistance. Moreover, it inhibits the growth of hPCSC tumors in an orthotopic xenograft mouse model.

Myristicin (Myristicine) is a natural product found in spices and umbelliferous plants. Myristicin has anti-cholinergic, Antibacterial, and hepatoprotective effects, it also has anti-inflammatory properties related with its inhibition of NO, cytokines,chemokines, and growth factors in dsRNA-stimulated macrophages via the calcium pathway. Myristicin can induce Apoptosis as characterised by alterations in the mitochondrial membrane potential, cytochrome c release, Caspase-3 activation, PARP-cleavage and DNA fragmentation.

L-Chicoric Acid (Standard) is a reference standard for research and analysis in studies involving L-Chicoric Acid. L-Chicoric Acid (trans-Caffeoyltartaric acid) has been shown to inhibit hyaluronidase and HIV-1 integrase, and to possess phagoeytosis stimulatory activity in vitro and in vivo and antiviral acitivy. L-Chicoric acid may reduce acute alcohol-induced steatosis in mice through interfering with the induction of iNOS and iNOS-dependent signaling cascades in the liver. 3. L-Chicoric acid inhibited cell viability and induced apoptosis in 3T3-L1 preadipocytes which was characterized by chromatin condensation and poly ADP-ribose-polymerase (PARP) cleavage.

Myristicin (Standard) is a reference standard for research and analysis in studies involving Myristicin. Myristicin (Myristicine) is a natural product found in spices and umbelliferous plants. Myristicin has anti-cholinergic, Antibacterial, and hepatoprotective effects, it also has anti-inflammatory properties related with its inhibition of NO, cytokines,chemokines, and growth factors in dsRNA-stimulated macrophages via the calcium pathway. Myristicin can induce Apoptosis as characterised by alterations in the mitochondrial membrane potential, cytochrome c release, Caspase-3 activation, PARP-cleavage and DNA fragmentation.