PARP Modulator

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.

Quinalizarin is a protein kinase CK2 inhibitor with a K_i 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.

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.

MKI-3 is a selective microtubule-associated serine/threonine kinase-like (MASTL) inhibitor with an IC₅₀ of 5.72 nM and a K_d 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.

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.

Continentalic acid (Standard) is the analytical standard of Continentalic acid (HY-N6908). This product is intended for research and analytical applications. 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.

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.

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.

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.

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.