2. Signaling Pathways
  3. Cell Cycle/DNA Damage
    Epigenetics
  4. PARP
  5. PARP Modulator

PARP Modulator

PARP Isoform Comparison

PARP Modulators (9):

Cat. No. Product Name Effect Purity
  • HY-163944
    LL-K12-18
    		Modulator 98.42%
    LL-K12-18 is a CDK12 kinase inhibitor and a dual-site molecular glue. LL-K12-18 inhibits human CDK12 with an IC50 value of 283.9 nM, and selectively degrades cyclin K via the ubiquitin-proteasome system by stabilizing the CDK12-DDB1 complex. LL-K12-18 downregulates DNA damage response genes, reduces the phosphorylation level of CTD Ser2 in RNA polymerase II, and modulates biomarkers such as ATM, RAD51, γ-H2AX and cleaved PARP, thereby effectively inducing apoptosis and inhibiting proliferation of breast cancer cells. LL-K12-18 exhibits high target selectivity and serves as a research tool for studies on triple-negative breast cancer.
  • HY-124833
    Quinalizarin
    		Modulator
    Quinalizarin is a protein kinase CK2 inhibitor with a Ki of 0.052 μM. Quinalizarin exhibits antifungal and anticancer activities. Quinalizarin induces ROS production, apoptotic signaling, mitochondrial pathway activation, cell cycle arrest, and cytotoxicity in cancer cells. Quinalizarin inhibits hyphal growth, biofilm formation, and mature biofilm integrity of Candida albicans. Quinalizarin can be used in research related to cancer and fungal infections.
  • HY-N6908
    Continentalic acid
    		Modulator 99.72%
    Continentalic acid is a diterpenoid organic acid. Continentalic acid exhibits multiple activities including anti-inflammatory, antioxidant, neuroprotective, antibacterial and antitumor effects. Continentalic acid alleviates oxidative stress, reduces pro-inflammatory cytokine production, inhibits MAPK phosphorylation and neutrophil infiltration, and induces growth inhibition and apoptosis of cancer cells. Continentalic acid can be used in research related to traumatic brain injury, cancer, inflammation and infections.
  • HY-183252
    ICA-1S
    		Modulator
    ICA-1S is a specific PKC-ι inhibitor. ICA-1S can inhibit MAPK/JNK signaling pathway and downregulate the levels of c-Jun and TNF-α. ICA-1S inhibits the proliferation of breast cancer cells. ICA-1S induces apoptosis of breast cancer cells. ICA-1S can be used in breast cancer-related research.
  • HY-182069
    CDK9-IN-47
    		Modulator
    CDK9-IN-47 is an orally active and selective CDK9 inhibitor with an IC50 of 1.4 nM. CDK9-IN-47 inhibits tumor cell proliferation, migration and invasion, and induces apoptosis. CDK9-IN-47 can be used for the research of triple-negative breast cancer.
  • HY-181084
    PROTAC BCL6/GSPT1 Degrader-1
    		Modulator
    PROTAC BCL6/GSPT1 Degrader-1 is a dual-target PROTAC degrader that targets BCL6 and GSPT1. PROTAC BCL6/GSPT1 Degrader-1 inhibits cell proliferation, promotes DNA damage, and induces cell cycle arrest and apoptosis in diffuse large B-cell lymphoma. PROTAC BCL6/GSPT1 Degrader-1 can be used for research on tumors such as lymphoma.
  • HY-182957
    MNK/PIM-IN-2
    		Modulator
    MNK/PIM-IN-2 is a Mnk/Pim kinase inhibitor with an IC50 of 32 nM for Mnk1, 3 nM for Mnk2, and 37 nM for Pim1. MNK/PIM-IN-2 reduces the levels of p-eIF4E and p-4EBP1. MNK/PIM-IN-2 induces cell cycle arrest, apoptosis (apoptosis) and exerts antiproliferative effects in leukemia cells. MNK/PIM-IN-2 can be used in studies related to leukemia.
  • HY-182391
    MKI-3
    		Modulator
    MKI-3 is a selective microtubule-associated serine/threonine kinase-like (MASTL) inhibitor with an IC50 of 5.72 nM and a Kd of 1.89 nM. MKI-3 disrupts the MASTL-ENSA-Aurora A signaling axis. MKI-3 induces chromosomal instability, mitotic catastrophe and apoptosis (apoptosis) in cancer cells. MKI-3 is applicable to research related to triple-negative breast cancer.
  • HY-182008
    NEURL1B-IN-1
    		Modulator
    NEURL1B-IN-1 is a molecular glue-like NEURL1B degrader with a Kd value of 46.2 nM. NEURL1B-IN-1 binds to Arg422 within the NHR2 domain of NEURL1B, triggers its autoubiquitination and proteasomal degradation, disrupts its interaction with DLL1, and attenuates the Notch signaling pathway. NEURL1B-IN-1 induces cell cycle arrest and apoptosis, and inhibits migration of hepatocellular carcinoma cells. NEURL1B-IN-1 is applicable to research related to hepatocellular carcinoma.