Caspase 7 Activator

Dehydrocorydaline (13-Methylpalmatine) is an alkaloid that regulates protein expression of Bax, Bcl-2; activates caspase-7, caspase-8, and inactivates PARP. Dehydrocorydaline elevates p38 MAPK activation. Anti-inflammatory and anti-cancer activities. Dehydrocorydaline shows strong anti-malarial effects (IC₅₀=38 nM), and low cytotoxicity (cell viability > 90%) using P. falciparum 3D7 strain.

HSP70-IN-9 is a Hsp70 inhibitor. HSP70-IN-9 activates Caspase-3 and -7. HSP70-IN-9 exerts anticancer effects against acute myeloid leukemia. HSP70-IN-9 can be used for the research of acute myeloid leukemia.

MS1129 is a DNMT degrader that induces proteasomal degradation of DNMT1, DNMT3A and DNMT3B proteins. MS1129 upregulates TRAIL, DR4 and DR5 proteins, downregulates the decoy receptor DcR2, and activates TRAIL-dependent apoptosis via the HIF-1/2 and Caspase-10 pathways. MS1129 is applicable to the research of VHL-deficient clear cell renal cell carcinoma.

RMC-4745 is a selective dual-site inhibitor of mTORC1, with a selectivity of 35 times for mTORC1 and mTORC2. RMC-4745 inhibits the proliferation of MCF-7 cells and upregulates Caspase-3/7 activity to induce cell apoptosis. RMC-4745 does not cause the upregulation of HER3 due to the inhibition of mTORC2. RMC-4745 can be used for the study of breast cancer.

TASIN-1 is a selective inhibitor of truncated APC^TR (adenomatous polyposis coli gene) that exerts cytotoxic effects by inhibiting cholesterol biosynthesis. TASIN-1 specifically targets colorectal cancer (CRC) cells carrying APC truncated mutations, while having no significant toxicity to wild-type APC cells. TASIN-1 exerts cytotoxic effects by targeting Emopamil binding protein (EBP) to inhibit cholesterol biosynthesis, triggering endoplasmic reticulum (ER) stress, reactive oxygen species (ROS) generation, and JNK-mediated apoptosis, and inhibiting Akt survival signaling. TASIN-1 can be used to prevent and intervene in APC mutant colorectal cancer.

Ligandrol is an orally active, selective androgen receptor (AR) agonist. Ligandrol enhances protein synthesis, inhibits muscle breakdown and oxidative stress, improves muscle cell viability and bone tissue microstructure, and reduces Cisplatin (HY-17394)-induced muscle toxicity and apoptosis. Ligandrol promotes muscle growth, protects bone structure, and has anti-diabetic, anti-apoptotic and antioxidant effects. Ligandrol can antagonize Streptozotocin (HY-13753) damage to pancreatic islets and improve the symptoms of type 2 diabetes.

JAB-2485 is an orally active and selective Aurora kinase A (AURKA) inhibitor with an IC₅₀ value of 0.327 nM. JAB-2485 exhibits inhibitory activity against various tumor cell lines such as neuroblastoma, triple-negative breast cancer, small cell lung cancer, and epithelial ovarian cancer. JAB-2485 can induce cell cycle arrest and apoptosis in tumor cells. JAB-2485 has antitumor activity.

Licoflavone C is a broad-spectrum antiviral inhibitor with estrogen-like properties. Licoflavone C binds to viral endonuclease (CEN) and inhibits the replication of various bunyaviruses including severe fever with thrombocytopenia syndrome virus (SFTSV) and lymphocytic choriomeningitis virus in a non-substrate competitive manner. The IC₅₀ values of Licoflavone C against SFTSV CEN and SFTSV CEN are 35.5 μM and 135.8 μM, respectively, and its K_d value against SFTSV CEN is 9.53 μM. After viral entry into cells, Licoflavone C reduces viral loads in mouse tissues in a dose-dependent manner, and exhibits extremely low cytotoxicity and genotoxicity. Licoflavone C induces apoptosis by increasing caspase 3/7 activity, blocks the cell cycle, and alleviates chemotherapy-induced chromosomal damage. Licoflavone C is applicable to the research on severe fever with thrombocytopenia syndrome and related viral infection mechanisms.

d-KLA Peptide (D-(KLAKLAK)2), KLA peptide (HY-P5345) isomer, is a pro-apoptosis peptide. d-KLA Peptide can specifically target mitochondria and induce apoptosis by destroying the mitochondrial membrane. d-KLA Peptide increases caspase 3/7 activity, exerts proapoptotic activity and enhances antitumor efficacy in mouse melanoma models.

PMV6-PEG4-BI2536 is an RIPTAC-like bifunctional molecule that promotes the formation of the p53^Y220C-PLK1 ternary complex (EC₅₀ = 1.4 μM). PMV6-PEG4-BI2536 causes PLK1 mislocalization and inhibits PLK1 activity, inducing G2/M phase arrest and apoptosis in p53^Y220C-mutant cells, while sparing cells with wild-type TP53. PMV6-PEG4-BI2536 can be used in research on uterine, gastric, pancreatic, prostate, and breast cancers harboring the p53^Y220C mutation. PMV6-PEG4-BI2536 is composed of PMV6 (a p53^Y220C mutant-binding ligand), PEG4 (a linker), and BI2536 (HY-159493) (a PLK inhibitor).

dCDK9-202 a potent CDK9 PROTAC degrader with an DC₅₀ value of 3.5 nM. dCDK9-202 exhibits broad-spectrum anti-tumor activity and extensively disrupts the oncogenic transcriptome. dCDK9-202 can activate Caspase-3/7, increase the level of cleaved PARP, and directly induce apoptosis of tumor cells. dCDK9-202 effectively inhibits TC-71 tumor growth without any signs of toxicity in mice. dCDK9-202 can be used for the study of EGFR-driven cancers such as sarcoma (Pink: CDK9 ligand (HY-178862); Blue: CRBN ligand (HY-W248665); Black: Linker (HY-N8015)).

2-Aminobenzothiazole acts as a caspase 3/7 activator, an anticancer cytotoxic agent, and also exhibits neurotoxicity. 2-Aminobenzothiazole drives the apoptotic pathway by activating caspase 3/7, induces mitochondrial inner membrane depolarization, and triggers both early and late apoptosis via a caspase-dependent pathway. In zebrafish models, 2-Aminobenzothiazole induces oxidative damage in brain tissues and inhibits genes related to GABA and 5-HT synthesis pathways. Long-term exposure to 2-Aminobenzothiazole impairs motor ability, social behavior, anxiety-like state and cognitive function. 2-Aminobenzothiazole can be used in studies of human laryngeal carcinoma and related neurotoxicity.

Fenobucarb is a carbamate insecticide. Fenobucarb induces zebrafish developmental neurotoxicity through pathways involved in inflammation, oxidative stress, degeneration and apoptosis. Fenobucarb is a possible risk factor to cardiovascular and cerebrovascular systems in animals.

TD1092 is a pan-IAP degrader, degrades cIAP1, cIAP2, and XIAP. TD1092 activates Caspase 3/7, and promotes cancer cells apoptosis via IAP degradation. TD1092 inhibits TNFα mediated NF-κB pathway and reduces the phosphorylation of IKK, IkBα, p65, and p38. TD1092 can act as PROTAC, and is used for cancer research.

Phlorizin (Floridzin) dihydrate is an orally active non-selective sodium-glucose cotransporter (SGLT) inhibitor, with an IC₅₀ of 0.04 μM and a K_i of 39 nM against hSGLT2, and an IC₅₀ of 0.17 μM and a K_i of 0.31 μM against hSGLT1. Phlorizin dihydrate promotes GLUT4 translocation, inhibits gluconeogenesis and promotes glycogen synthesis by activating the PI3K/Akt/mTOR pathway. Phlorizin dihydrate reduces DNA damage and apoptosis (apoptosis) by inhibiting the NF-κB inflammatory pathway. Phlorizin dihydrate induces apoptosis via activating the Caspase pathway by antagonizing the JAK/STAT3 and PCK pathways. Phlorizin dihydrate also exhibits antibacterial, anti-inflammatory and neuroprotective activities.

Nodularin is a hepatotoxin, tumor promoter, and protein phosphatase inhibitor. Nodularin induces apoptosis (apoptosis) in normal cells (including caspase activation, upregulation of Bcl‑XS, and upregulation of BAX/P53), triggers hyperphosphorylation of the MAPK/ERK, mTOR/S6K and p38 MAPK signaling pathways, and induces oxidative stress, endoplasmic reticulum membrane instability, peroxisome proliferation and increased lysosomal enzyme activity. Nodularin promotes DEN (HY-N7434)-initiated hepatocyte proliferation and adenoma formation, and inhibits proliferation, phagocytosis and chemotaxis of normal lymphocytes, oocyte maturation and vitellogenesis, as well as angiogenesis. Nodularin exhibits hepatotoxicity, reproductive and endocrine toxicity, and embryonic developmental toxicity in various animal models. Nodularin can be used in studies related to liver cancer, hepatotoxicity and reproductive endocrine toxicity.

PROTAC K-Ras Degrader-5 is a cereblon-based K-Ras PROTAC degrader with a DC₅₀ of <100 nM for KRAS^G12D. PROTAC K-Ras Degrader-5 recruits KRAS^G12D to the cereblon E3 ubiquitin ligase complex for ubiquitination and subsequent proteasomal degradation. PROTAC K-Ras Degrader-5 suppresses pERK levels downstream of KRAS^G12D degradation in cancer cells. PROTAC K-Ras Degrader-5 reduces proliferation of cancer cells. PROTAC K-Ras Degrader-5 induces caspase 3/7 activity and cPARP, markers of apoptosis, in pancreatic cancer spheroids and tumors. PROTAC K-Ras Degrader-5 can be used for the research of pancreatic cancer and colorectal cancer.

PAWI-2 is a p53-Activator and Wnt Inhibitor. PAWI-2 inhibits β3-KRAS signaling independent of KRAS. PAWI-2 selectively inhibits phosphorylation of TBK1. PAWI-2 activates apoptosis (activation of caspase-3/7), and induces PARP cleavage. PAWI-2 promotes optineurin translocation into the nucleus and causes G2/M arrest. PAWI-2 reverses cancer stemness and overcomes drug resistance in an integrin β3 KRAS-dependent human pancreatic cancer stem cells (hPCSCs). PAWI-2 inhibits growth of tumors from hPCSCs in orthopic xenograft mice model.

LD5097 is a highly effective and selective PROTAC degrader targeting RIPK1. LD5097 can rapidly and efficiently downregulate RIPK1 and significantly enhance TNFα-mediated apoptosis in Jurkat cells. LD5097 significantly increases the levels of cleaved caspase-3/7 and PARP. LD5097 can be used for the study of acute T-lymphoblastic leukemia.

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.