PARP

Lerzeparib is an (ADP-ribose) polymerase (PARP) inhibitor, with antineoplastic activity.

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 .

Topoisomerase I/II Inhibitor 8 (Compound Ru7) is a dual catalytic inhibitor of Topoisomerase I/II, capable of inducing DNA damage and PARP-1 activation, which subsequently leads to the activation of RIPK1, RIPK3, and MLKL, ultimately triggering necroptosis. Topoisomerase I/II Inhibitor 8 demonstrates remarkable anticancer activity by effectively targeting the nuclei of cancer cells and inducing cell death through necroptosis, showing great clinical potential in circumventing drug resistance in cancer treatment.

PARP1-IN-9 (Compound 5c) is a PARP1 inhibitor with an IC₅₀ of 30.51 nM. PARP1-IN-9 induces cell apoptosis and shows anticancer activity. PARP1-IN-9 has higher potency than Olaparib (HY-10162) .

PARP1 Ligand-linker Conjugate-1 is a PARP1 ligand-linker conjugate that can be used for the synthesis of PROTACs, such as CW-2 (HY-173437).

PARP-2-IN-3 (Compound 12) is a potent PARP-2 inhibitor with an IC₅₀ of 0.07 μM. PARP-2-IN-3 induces apoptosis and necrosis in cancer cells. PARP-2-IN-3 shows appropriate predicted pharmacokinetic parameters and oral bioavailability.

AC-45594 (4-(Hexyloxy)phenol) is a UPR activator. AC-45594 induces endoplasmic reticulum stress, activates the unfolded protein response (UPR), and drives the transition from adaptive stress signaling to terminal stress signaling, ultimately leading to cell Apoptosis. AC-45594 activates Caspase-3, induces PARP cleavage, and increases the protein level of DR5. AC-45594 selectively inhibits the growth of Ewing sarcoma cells.

Quinidine gluconic acid is an orally active antiarrhythmic agent. Quinidine gluconic acid 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 gluconic acid exerts sustained block and open-channel block effects on I_K(f). Quinidine gluconic acid alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine gluconic acid can be used in studies related to uterine sarcoma and seizures.

PARP1-IN-49 is a selective PARP1 inhibitor with an IC₅₀ of 23.56 nM and a K_d of 17.78 nM. PARP1-IN-49 shows a selectivity for PARP1 over PARP2. PARP1-IN-49 leads to the induction of DNA damage, cell cycle arrest, and apoptosis. PARP1-IN-49 also increases intracellular ROS levels and inhibits cell migration. PARP1-IN-49 can be used for the research of breast cancer and ovarian cancer.

Jujuboside B (Standard) is the analytical standard of Jujuboside B. This product is intended for research and analytical applications. Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.

PARP1-IN-42 (Example 43 cis-a) is a PARP1 inhibitor with IC₅₀ <10 nM. PARP1-IN-42 can be used in cancer research.

TNKS1/2-IN-2 (Compound 21) is a potent and selective tankyrases inhibitor. TNKS1/2-IN-2 exhibits IC₅₀ values of 4 nM and 63 nM against TNK1 and TNK2 in the enzymatic assay, respectively. TNKS1/2-IN-2 inhibits proliferation of A549 and H292 cell lines with IC₅₀ values of 39.5 nM and 12.8 nM, respectively. TNKS1/2-IN-2 can be used for the research of cancer.

PARP1/PKM2-IN-1 is a dual PARP1/PKM2 inhibitor, with an IC₅₀ of 39.5 nM against PARP1, and IC₅₀ values of 261 nM (recombinant PKM2) and 50 nM (dimeric PKM2) against PKM2. PARP1/PKM2-IN-1 reduces the dimerization of PKM2 and decreases its nuclear accumulation level. PARP1/PKM2-IN-1 also selectively downregulates PKM2 mRNA and impairs poly (ADP-ribose)-mediated nuclear retention of PKM2. PARP1/PKM2-IN-1 exhibits antiproliferative activity and inhibits the formation of 3D cancer spheroids. PARP1/PKM2-IN-1 can be used in research related to mammary adenocarcinoma, triple-negative breast cancer, BRCA1-mutant triple-negative breast cancer, and prostate adenocarcinoma.

Anticancer agent 137 (8q) is a potent PI3k inhibitor. Anticancer agent 137 has broad-spectrum anticancer activity. Anticancer agent 137 induces G2/M cell cycle arrest and apoptosis. Anticancer agent 137 increases cleaved PARP, caspase 3, and 7. Anticancer agent 137 can be used in research of cancer.

OM-1700 is a potent tankyrase inhibitor with IC₅₀s of 127 and 14 nM for tankyrase 1 and tankyrase 2, respectively. OM-1700 reduces cell growth in the colon cancer cell line COLO 320DM (GI₅₀=650 nM).

TOPOI/PARP-1-IN-2 (compound 6c) is a dual PARP-1 and topoisomerase 1 (TOPO-1) inhibitor with IC₅₀s of 32.2 nM and 46.2 nM, respectively. TOPOI/PARP-1-IN-2 shows a selectivity for PARP-1 over PARP-2. TOPOI/PARP-1-IN-2 disrupts the cell cycle at the S phase and induces apoptosis in NCI-60 cancer cell lines.

Sargachromanol E is an apoptosis inducer, anti-inflammatory agent, and anti-aging agent. Sargachromanol E activates caspase-3, mediates PARP cleavage, downregulates Bcl-xL and upregulates Bax levels, and drives sub-G1 phase cell cycle arrest, inhibits LPS-induced COX-2 and iNOS transcription and expression (NO: IC₅₀ = 6.99 μg/mL), reduces p38 MAPK and ERK1/2 phosphorylation levels, and suppresses the release of pro-inflammatory mediators such as TNF-α, IL-1β, and prostaglandin E₂ (PGE₂). Sargachromanol E can be used for research on skin aging, leukemia, oral squamous cell carcinoma, and inflammation-related studies.