Apoptose

<p>Flizasertib is a serine/threonine kinase inhibitor that acts by inhibiting RIPK1, which has anti-inflammatory and therapeutic effects on immune disorders.</p>

<p>FLT3-ITD-IN-3 (13v) is an orally active inhibitor of FLT3-ITD (internal tandem duplication of FLT3), which works by blocking FLT3 signaling. This inhibition leads to cell cycle arrest in the G0/G1 phase and induces apoptosis. The compound is currently employed in studies related to acute myeloid leukemia (AML).</p>

<p>AZD0424: oral Src/Abl kinase inhibitor; potential anticancer; induces apoptosis, cell cycle arrest in lymphoma.</p>

<p>Nenocorilant (Relacorilant) is an orally active glucocorticoid receptor (GR) antagonist (Ki: 0.15 nM). Nenocorilant can be used to study tumours.</p>

<p>SMIP34 is an inhibitor of PELP1, binding to this target with a dissociation constant (Kd) of 37.4 μM. It demonstrates efficacy in inhibiting the proliferation of cancer cells and tumor progression. Specifically, SMIP34 is effective in breast cancer research, showing activity against wild-type (WT), mutant (MT) estrogen receptor-positive (ER+), and treatment-resistant (TR)-ER+ breast cancers.</p>

<p>PD-1/PD-L1-IN-15 is a potent inhibitor of PD-1/PD-L1 (IC50: 60.1 nM) and has shown investigational potential for tumor immunotherapy.</p>

<p>BCL6-IN-9 (compound 1) is a potent inhibitor of B-cell lymphoma 6 protein (BCL6) (IC50: 3.9 nM) and can be used to study cancer.</p>

<p>VEGFR-IN-3 inhibits cancer cell growth (OVCAR-4, MDA-MB-468) with IC50s: 0.29, 0.35μM. Used in cancer research.</p>

<p>Anticancer agent 14: a potent breast cancer inhibitor; induces cell death, disrupts mito. membrane potential (IC50: 0.20-0.65 μM).</p>

<p>Microtubulin-IN-1 (Compound 8g) is an inhibitor of microtubulin, targeting the colchicine-binding site to disrupt tubulin integrity and induce upregulation of p53 protein expression. It exhibits antiproliferative activity across various cancer cell lines, including NCI-H460, BxPC-3, and HT-29, with IC50 values of 2.4, 1.6, and 2.07 nM, respectively. Additionally, Microtubulin-IN-1 induces cell cycle arrest at the G2/M phase and apoptosis in NCI-H460 cells.</p>

<p>DPP-21 is an inhibitor of microtubule protein polymerization (IC50: 2.4 μM). It exhibits antiproliferative activity against various cancer cell lines, with IC50 values of 0.38 nM (HCT116), 11.69 nM (B16), 5.37 nM (HeLa), 9.53 nM (MCF7), 8.94 nM (H23), and 9.37 nM (HepG2). DPP-21 induces cell cycle arrest at the G2/M phase of mitosis and subsequently triggers apoptosis in tumor cells by decreasing Bcl-2 while increasing pro-apoptotic protein Bax levels.</p>

<p>Antitumor agent-202 is a stabilizer of the p53Y220C mutant, selectively inhibiting the proliferation of tumor cells carrying the p53Y220C mutation. It is applicable for research focused on cancers associated with the p53 Y220C mutation.</p>

<p>LA-CB1 is a derivative of Abemaciclib that targets CDK4/6 and promotes their degradation via the ubiquitin-proteasome pathway, thereby blocking the CDK4/6-Cyclin D1-Rb-E2F axis and inducing G0/G1 cell cycle arrest and apoptosis (Apoptosis). It demonstrates antiproliferative activity against MDA-MB-231 cells with an IC50 of 0.27 µM and effectively inhibits epithelial-mesenchymal transition, cell migration, invasion, and angiogenesis. In highly invasive models like triple-negative breast cancer (TNBC), LA-CB1 significantly suppresses tumor growth, showing robust dose-dependent antitumor activity. This compound can be utilized in breast cancer research.</p>

<p>Cetzole (Compound 1) acts as an inducer of ferroptosis (iron-dependent cell death) through the accumulation of ROS, leading to cell death. The compound exhibits varying half-maximal cytotoxic concentrations (CC50) against several cell lines: 2.56 μM in NCI-H522, 10.31 μM in NCI-H522 GFP-SCL7A11 #8, 2.71 μM in NCI-H522 RV-GFP, 3.07 μM in HT-1080, 14.9 μM in NARF2, and 6.28 μM in MDA-MB-231. This highlights Cetzole's potential for research in cancer therapeutics.</p>

<p>TFCP2L1-IN-1 is a TFCP2L1 transcription factor inhibitor that regulates cell proliferation and promotes antitumor effect of Sorafenib by STAT3/NANOG pathway.</p>

<p>Claturafenib is a brain-permeable, selective, all-mutant BRAF inhibitor.PF-07799933 has shown antitumor activity, used in combination with MEK inhibitors.</p>

<p>CDK2/9-IN-1 (compound 20a) is an orally active dual inhibitor of CDK2 and CDK9, with IC50 values of 0.004 μM and 0.009 μM for CDK2 and CDK9, respectively. It induces apoptosis by regulating G2/M cell cycle arrest and exhibits antitumor activity.</p>

<p>NA-17 is a naphthalimide compound with antitumor activity and exhibits lower toxicity to normal cells such as HL-7702 and WI-38. It demonstrates p53-dependent inhibition selectivity in various NSCLC cells, inducing the accumulation of active p53 in the mitochondria and nuclei of these cells. NA-17 causes cell cycle arrest in the G1 phase and promotes apoptosis and cell death.</p>

<p>Mcl-1 Inhibitor 9 (Example 2) is a potent inhibitor of myeloid cell leukemia 1 (Mcl-1), demonstrating anti-tumor activity with an IC50 value of 0.21889 nM.</p>

<p>Z-VAD is an irreversible pan-caspase inhibitor, suppressing multiple caspases including caspase-3, -6, -7, -8, and -9. Z-VAD induces autophagy in tumour cells.</p>

<p>Antiproliferative agent-4 suppresses cancer cell growth with low toxicity, inhibits tumors in mice, and induces apoptosis in EC109 cells.</p>

<p>AKN-028 acetate: an oral TK inhibitor for AML research, targets FLT3 with IC50 of 6 nM, inhibits autophosphorylation, and induces apoptosis.</p>

<p>K20 selectively inhibits KRas G12C (IC50: 1.16 nM), shows anticancer activity in H358 cells (IC50: 0.78 μM), and induces apoptosis via Erk dephosphorylation.</p>

<p>mTOR/HDAC6-IN-1 inhibits HDAC6 (IC50: 56 nM) &amp; mTOR (IC50: 133.7 nM), may treat TNBC by inducing autophagy and apoptosis.</p>

<p>CHI-KAT8i5 is a selective inhibitor of KAT8 with a KD of 19.72 μM. It induces apoptosis (Apoptosis) in a dose-dependent manner. CHI-KAT8i5 can inhibit tumor growth in esophageal squamous cell carcinoma, colon cancer, melanoma, gastric cancer, non-small cell adenocarcinoma, and liver cancer.</p>

<p>Topo I/COX-2-IN-1: potent dual inhibitor; IC50 0.24μM (COX-2), 4.42μM (Topo I); anti-cancer; induces apoptosis, halts migration.</p>

<p>VEGFR-2-IN-15 (Compound 14b) is a potent inhibitor of VEGFR-2. VEGFR-2-IN-15 inhibits the growth of HepG2 cells in the Pre-G1 phase and induces apoptosis.</p>

<p>DL-Buthionine-(S,R)-sulfoximine hydrochloride (Buthionine sulfoximine hydrochloride) is a potent and specific glutamylcysteine synthetase biosynthesis inhibitor</p>

<p>[D-Leu-4]-OB3 suppresses the expression of genes associated with inflammation, proliferation, and metastasis, as well as the expression of PD-L1.</p>

<p>Antitumor Agent-184 (compound 12aa) triggers apoptosis in various cell lines, exhibiting IC50 values of 2.35 μM in B16-F10 cells, 7.32 μM in 4T1 cells, and 10.31 μM in CT26 cells.</p>

<p>Glyphosate isopropylammonium is a broad-spectrum, non-selective systemic biocide derived from the amino acid glycine. It inhibits the enzyme activity of 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) in the shikimate pathway, blocking the synthesis of aromatic amino acids tyrosine, phenylalanine, and tryptophan. Additionally, Glyphosate isopropylammonium induces oxidative stress, neuroinflammation, and mitochondrial dysfunction, leading to neuronal death through autophagy, necrosis, or apoptosis, resulting in behavioral and motor disturbances.</p>

<p>Topo II/HDAC-IN-1 (7d) demonstrates potent dual inhibitory effects on Topo II and HDAC, while Topo II/HDAC-IN-1 (8d) effectively induces apoptosis [1].</p>

<p>TI17 is a selective TRIP13 inhibitor with anticancer activity and inhibits proliferation of multiple myeloma (MM) cells</p>

<p>Necrosis Inhibitor 3 (compound B3) effectively inhibits necrosis, demonstrating an IC50 of 0.29 nM in HT29 cells [1].</p>

<p>GQN-B37-E is an effective selective binder and inhibitor of MCL-1. It binds to the BH3-binding domain of MCL-1. GQN-B37-E demonstrates binding affinity for MCL-1 within the sub-micromolar range (Ki= 0.6 μM), yet shows negligible binding to BCL-2 or BCL-XL.</p>

<p>Mcl-1 inhibitor21 (Example 1-36) is an Mcl-1 inhibitor with an IC50 of 328 nM. It exhibits pro-apoptotic and anti-proliferative activity against SUDHL5 and SUDHL10 cell lines, making it applicable for cancer research.</p>

<p>MJC13 is an FKBP52-targeting agent with antitumor activity, suitable for prostate cancer research.</p>

<p>3′-Hydroxyflavanone is a cyclized flavonoid with anti-tumor properties that induces apoptosis in HeLa cells.</p>

<p>Compound 5f, a potent tubulin polymerization inhibitor (IC50 = 1.09 μM), blocks cell migration, tube formation, and has anti-angiogenic effects.</p>

<p>PD-1/PD-L1-IN-16 is a potent inhibitor of PD-1/PD-L1 (IC50: 53.2 nM) and has shown research potential for tumour immunotherapy.</p>

<p>Etalocib (LY293111) sodium is an orally active leukotriene B4 (LTB4) receptor antagonist with a Ki value of 25 nM for inhibiting [3H]LTB4 binding. It exhibits an IC50 of 20 nM against LTB4-induced calcium mobilization. Additionally, Etalocib sodium can induce apoptosis.</p>

<p>ASP9831 is an orally active PDE4 inhibitor. It suppresses LPS-induced TNF-α production and exhibits anti-inflammatory properties. ASP9831 is useful in the study of steatohepatitis.</p>

<p>PD-L1/VISTA-IN-1 (Compound P17) is an orally active dual inhibitor targeting PD-L1 and VISTA. It effectively hinders the PD-1/PD-L1 interaction (IC50: 0.1492 μM) and the VISTA pathway (KD: 0.2723 μM), leading to the reactivation of T cells. Additionally, PD-L1/VISTA-IN-1 exhibits antitumor activity.</p>

<p>Sinulatumolin E, a terpenoid, inhibits TNF-α (IC 50: 3.6 μM); has anti-inflammatory properties.</p>

<p>XPO1-IN-1: an oral MM.1S cell inhibitor (IC50: 24 nM), induces apoptosis, stable metabolism, good pharmacokinetics.</p>

<p>Belotecan (CKD-602) inhibits DNA topoisomerase I, blocks cell cycle, induces apoptosis, and is a camptothecin-derived anticancer agent.</p>

<p>TP-030-1, RIPK1 inhibitor: K(i) hRIPK1 at 3.9nM, IC50 mRIPK1 at 4.2μM; targets inflammation, neurodegeneration research.</p>

<p>Nur77 agonist-1 (Compound 8f) is an orally active Nur77 agonist. It induces ferroptosis by upregulating Nur77 protein expression, increasing reactive oxygen species (ROS) and lipid peroxidation levels, while decreasing GPX4 protein expression. Nur77 agonist-1 binds with affinity to the ligand binding domain of Nur77, with a KD of 13.80 μM. It demonstrates significant antiproliferative activity against various breast cancer cells (IC50: 2.15-3.26 μM) and exhibits low cytotoxicity towards normal cells. This compound is useful for breast cancer research.</p>

<p>HC-5404-Fu is an inhibitor of PERK with anti-tumor activity. This compound inhibits the signaling pathway of the endoplasmic reticulum stress response. Additionally, HC-5404-Fu increases the sensitivity of renal cell carcinoma cells to vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors (TKIs). It holds potential for research into renal cell carcinoma, stomach cancer, metastatic breast cancer, small cell lung cancer, and other solid tumors.</p>

<p>SPI-001 is a selective inhibitor of PPM1D (IC50=0.48 µM) that exhibits anticancer activity. The compound inhibits the phosphatase activity of PPM1D in human breast cancer cells overexpressing PPM1D and enhances the phosphorylation of p53. Additionally, SPI-001 suppresses cell proliferation by inducing apoptosis.</p>

<p>Triphen diol, a phenol diol, fights pancreatic cancer &amp; cholangiocarcinoma, inducing apoptosis via caspase-dependent &amp; -independent paths.</p>

<p>PIM1-IN-3 (HL8) selectively blocks PIM1, induces Colo320 cell apoptosis, and may be researched for cancer.</p>

<p>BMI-135, a selective estrogen mimic, demonstrates agonist activity for the estrogen receptor and induces a rapid endoplasmic reticulum stress response (UPR) alongside apoptosis in breast cancer cells.</p>

<p>Apoptosisinducer 25 (Compound 4H) demonstrates potent anticancer capabilities by inhibiting the proliferation of BGC-823 cancer cells with an IC50 of 0.37 μM. It induces apoptosis in BGC-823 cells, causes mitochondrial dysfunction, and arrests the cell cycle at the G2/M phase. Additionally, Apoptosisinducer 25 exhibits favorable pharmacokinetic properties in rats.</p>

<p>Anticancer agent 44 induces apoptosis, is selective, cytotoxic to cancer cells, and minimally toxic to human lymphocytes.</p>

<p>17-Demethoxy-reblastatin (17-DR) acts as an inhibitor of heat shock protein 90 (Hsp90). It suppresses the proliferation of HepG2 and SMMC7721 cancer cells, diminishes colony formation, and triggers apoptosis via a mitochondria and caspase-mediated pathway.</p>

<p>N-ω-chloroacetyl-L-ornithine (NCAO) serves as a powerful reversible competitive inhibitor of ornithine decarboxylase (ODC), displaying cytotoxic and antiproliferative properties against various tumor cell lines, with EC50 values spanning from 1 to 50.6 µM. In vitro studies reveal that NCAO promotes Apoptosis and restricts tumor cell migration. Additionally, it demonstrates significant antitumor efficacy in a mouse model, targeting both solid and ascitic tumors using the myeloma (Ag8) cell line. NCAO holds promise in the development of antitumor agents.</p>

<p>p53 Activator 14 (Compound 7A) is a derivative of Neratinib that can induce DNA damage and activate p53, thereby inhibiting the proliferation of various cancer cells, with an IC50 of 7.21 μM for HCT116 cells. This compound hinders adhesion, migration, and invasion of HCT116 cells, disrupts the cell cycle, and triggers apoptosis. In addition, p53 Activator 14 exhibits anti-tumor properties and inhibits angiogenesis in the chick embryo chorioallantoic membrane (CAM) model.</p>

<p>Thalidomide-NH-amido-PEG2-C2-NH2 is a synthetic E3 ligase ligand-linker conjugate comprising a Thalidomide-based cereblon ligand and a linker. It is utilized in the synthesis of PROTACs.</p>

<p>WK88-1, an inhibitor of Hsp90, effectively induces the degradation of various oncogenic signaling molecules, including EGFR, ErbB2, and ErbB3, in the gefitinib-resistant H1975 cell line. This leads to subsequent growth arrest and apoptosis.</p>

<p>Compound Z15 (ZNU-IMB-Z15) acts as an antagonist and degrader of the androgen receptor (AR). It inhibits the proliferation of castration-resistant prostate cancer (CRPC) cell lines that are AR-positive and induces apoptosis. Compound Z15 exhibits anticancer activity both in vivo and in vitro.</p>

<p>TLBC, a borane-chalcone derivative, exhibits dose-dependent inhibitory effects across various glioma cell lines with IC50 values ranging from 5.5 to 25.5 μM. TLBC induces apoptosis independently of alterations in the tumor suppressor factor p53.</p>

<p>Ph-Ph+ is a dimerized phenanthroline derivative with antitumor, antibacterial, and antifungal effects.</p>

<p>Antiproliferative agent-63 (compound 4d) is a cyclic analog of cannabidiol that acts as an anticancer agent. It demonstrates favorable activity against breast and colorectal cancer. Moreover, this compound can arrest the cell cycle in the G1 phase and induce apoptosis through the mitochondrial pathway in breast cancer cell lines.</p>

<p>EGFR-IN-45: Strong EGFR/CDK2 inhibitor (IC50s: 0.4 &amp; 1.6 μM), halts cancer cell cycle pre-G1, prompts apoptosis, also targets Topo I/II.</p>

<p>Anticancer agent 65: Effective on A549 cells, IC50 1.07 μM, halts S phase, triggers apoptosis, elevates p53/p21, causes ROS and MMP collapse.</p>

<p>SIRT-IN-7 (Compound 7ba) is a SIRT inhibitor. It effectively suppresses the expression of SIRT1, SIRT2, and SIRT3, leading to increased acetylation and activation of p53. Additionally, SIRT-IN-7 inhibits the proliferation of breast cancer cells and induces apoptosis and autophagy, demonstrating antitumor activity.</p>

<p>D18: Dual agonist for TLR7/8, boosts PD-L1, aids tumor sensitivity to PD-1/PD-L1 inhibitors, and is a cytotoxin for ADC HE-S2.</p>

<p>SphK1-IN-2: SphK1 inhibitor, IC50: 19.81 nM; less effective on SphK2. Induces apoptosis, hinders cancer cell growth.</p>

<p>Verrucarin A, a mycotoxin from Myrothecium verrucaria, inhibits protein synthesis, leukemia growth, and triggers apoptosis.</p>

<p>Anticancer agent 53 exhibits potent in vitro cytotoxicity, triggers apoptosis, halts S/G2/M cycle, and has antitumor effects without toxicity.</p>

<p>L-threo-Sphingosine C-18 is a protein kinase C inhibitor.</p>

<p>D-Cl-amidine hydrochloride is a potent and highly selective inhibitor of PAD1. It exhibits excellent tolerance and does not induce significant toxicity [1].</p>

<p>c-Myc inhibitor16 iodide (Compound W11) is a selective inhibitor of the c-MycG-quadruplex (c-MycG4). It suppresses the transcription and translation of the c-Myc gene, disrupts the tumor cell cycle by halting growth at the G0/G1 phase, and activates mitochondrial apoptotic pathways, leading to early apoptosis in cancer cells. This compound shows potential for research in breast cancer.</p>

<p>PLK1-IN-13 is a selective, orally active PLK1 inhibitor with an IC50 of 0.27 nM. It also inhibits PLK2 (IC50: 12.72 nM) and PLK3 (IC50: 4.12 nM). PLK1-IN-13 induces cell cycle arrest at the G2 phase, promotes apoptosis, and downregulates the transcription of the cancer-associated oncogene c-MYC. This compound inhibits tumor growth and is applicable for research in acute myeloid leukemia (AML).</p>

<p>ZLHQ-5f inhibits CDK2/Topo I, with IC50 of 0.145μM for CDK2/CycA2, and promotes apoptosis by arresting HCT116 cells in S phase.</p>

<p>p53 Stabilizer 2 (Compound 17a16) is a p53 stabilizing agent. It can induce S-phase arrest and apoptosis in both p53-functional and p53-deficient cancer cells. Additionally, p53 Stabilizer 2 triggers mitochondrial stress and activates two immune checkpoint pathways: NA-PKcs dependent p53 stabilization and the ATR-Chk1 axis activation. It also inhibits tumor growth in p53-deficient xenograft models.</p>

<p>Anticancer agent 64 (5m) induces apoptosis, has IC50 2.4μM in CCRF-CEM, activates caspases, cleaves PARP, affects mitochondria.</p>

<p>GRP78-IN-1 binds to GRP78 protein, inhibits cell growth, and triggers apoptosis in breast cancer; has -8.07 kcal/mol binding energy.</p>

<p>PAK4-IN-5 (Compound 12i) is a potent inhibitor of PAK4 (IC50: PAK4 at 7.68 nM, PAK1 at 1872.01 nM) that forms stable interactions with the PAK4 enzyme. This compound effectively inhibits the proliferation and migration potential of MDA-MB-231 cells by hindering the phosphorylation of PAK4 and LIMK1. Additionally, PAK4-IN-5 arrests the cell cycle in the G0/G1 phase, induces apoptosis, and prompts the production of reactive oxygen species. The LD50 in mice is greater than 500 mg/kg (oral).</p>

<p>Topoisomerase IIα-IN-4 (F2) is a non-intercalative ATP-competitive inhibitor of human DNA topoisomerase II, specifically inhibiting TopoIIα with an IC50 value</p>

<p>Multi-kinase-IN-1, a powerful kinase inhibitor, exhibits antitumor properties by inducing cell apoptosis.</p>

<p>MA242 free base is a dual MDM2/NFAT1 inhibitor that triggers apoptosis in pancreatic cancer cells.</p>

<p>ERK1/2 inhibitor 11 (compound L6) is a dual inhibitor of ERK1/2 that promotes the accumulation of DSBs and the degradation of ERK1/2 expression. This compound decreases BCL-2 levels and induces DNA damage by inhibiting PARP and ERK1/2. Additionally, ERK1/2 inhibitor 11 activates caspase 3 to induce apoptosis.</p>

<p>Compound 3 (DOR agonist 2) acts as a Delta Opioid Receptor agonist. It inhibits the expression of TNF-α, obstructs NF-κB transportation to the nucleus, and activates the G protein-mediated ERK1/2 pathway. This compound is useful for research into neurodegenerative diseases.</p>

<p>Potent oral XIAP/cIAP1 inhibitor with EC50s: XIAP 5.1 nM, cIAP1 0.32 nM; curbs tumor growth in vivo.</p>

<p>Metamizole (Dipyrone) hemimagnesium is an anti-inflammatory and antioxidant compound known for its ability to reduce fever. It decreases levels of C-reactive protein (CRP) and interleukin 6 (IL-6). Additionally, Metamizole hemimagnesium acts as an orally active cyclooxygenase (COX) inhibitor, suppressing cell proliferation and promoting apoptosis. It is utilized in the study of inflammation and fever.</p>

<p>GLI1-IN-1 (CBC-1), a GLI-1 inhibitor, exhibits superior water solubility and anticancer properties. It effectively induces apoptosis and inhibits colorectal cancer growth by targeting the Hedgehog (HH) pathway (IC 50 = 1.3 μM) [1].</p>

<p>Fluvastatin (XU 62-320) sodium monohydrate, a fully synthetic competitive HMG-CoA reductase inhibitor, features an IC 50 of 8 nM. This compound also safeguards vascular smooth muscle cells from oxidative stress via the Nrf2-dependent antioxidant pathway [1] [2].</p>

<p>Anticancer agent 54 blocks cell cycle in G0/G1, induces apoptosis, and fights cancer via DNA embedding and ROS.</p>

<p>PDEδ/NAMPT IN-1 (Compound 17d) is a dual inhibitor targeting phosphodiesterase 6 (PDE6) with a dissociation constant (KD) of 0.410 nM and nicotinamide phosphoribosyltransferase (NAMPT) with an inhibitory concentration (IC50) of 2.21 nM. It disrupts KRAS-related signaling by inhibiting NAMPT's role in the synthesis of nicotinamide adenine dinucleotide (NAD+), consequently inducing apoptosis in pancreatic cancer cells with KRAS mutations. This compound holds potential for research in KRAS-mutant pancreatic cancer.</p>

<p>microRNA-21-IN-1: microRNA inhibitor, curbs HeLa/HCT-116 growth (IC50: 5.5/2.8 μM), induces HeLa apoptosis, elevates PTEN/EGR1/SLIT2, for cancer research.</p>

<p>VEGFR-2-IN-18 is a potent VEGFR-2 inhibitor with a 60 nM IC50, promoting cell apoptosis and anticancer effects.</p>

<p>ER covalent antagonist-1 (Compound 39D) acts as an antagonist of the estrogen receptor α (ERα). This compound inhibits the proliferation of ERα-positive MCF-7 cells with an IC50 of 0.98 μM, induces cell cycle arrest at the G0/G1 phase, and triggers apoptosis. Additionally, ER covalent antagonist-1 demonstrates antitumor activity in mouse models.</p>

<p>WEHI-9625 is a tricyclic sulfone small molecule apoptosis inhibitor (EC50: 69 nM).</p>

<p>PD-1-IN-17 TFA is a potent PD-1 inhibitor, blocking 92% of splenocyte growth at 100 nM.</p>

<p>HDAC-IN-37 inhibits HDACs 1, 3, 8, &amp; 6, induces histone acetylation, halts G1 to S phase, and triggers early apoptosis.</p>

<p>MLS-0053105, a chloromaleimide, functions as a selective inhibitor of BFL-1, exhibiting an IC50 of 0.4 µM against Bfl-1/F-Bid. Its inhibitory potency is over tenfold lower for Bcl-W, Bcl-2, and Bcl-XL, and it shows no activity against Bcl-B and Mcl-1.</p>

<p>N-a-Tosyl-L-lysinyl-chloromethylketone hydrochloride (TLCK hydrochloride) is an irreversible serine protease inhibitor that functions by alkylating the histidine residue at the active site, thus inhibiting trypsin and trypsin-like proteases. It effectively inhibits caspase-3, caspase-6, and caspase-7 with IC50 values of 12.0, 54.5, and 19.3 μM, respectively. Additionally, N-a-Tosyl-L-lysinyl-chloromethylketone hydrochloride induces apoptosis in HL-60 cells and prevents the reduction of mitochondrial transmembrane potential during the apoptosis process.</p>

<p>L5-DA, a G-quadruplex ligand, stabilizes G4s in HeLa cells, induces apoptosis, and is cytotoxic with an IC50 of 4.3 μM.</p>

<p>tDHU, acid is a dihydropyrimidine cereblon ligand consisting of an E3 ligase ligand and a benzoic acid linker. It serves as an E3 ubiquitin ligase ligand-linker conjugate in the development of PROTACs.</p>

<p>Tubulin inhibitor 14 blocks NQO2 and microtubule formation, disrupts blood vessels, and may target tumors; IC50 of 1.0 μM.</p>

<p>Fosizensertib is an inhibitor of RIP-1 kinase and is used in research related to ulcerative colitis.</p>

<p>Z-VA-DL-D-FMK (Z-VA-DL-D(OH)-FMK) acts as an inhibitor of caspases. It irreversibly binds to caspases, enhancing the sensitivity to TNF-α and stimulating HIV replication in infected T cells ACH-2.</p>

<p>EGFR-IN-47: strong oral EGFRL858R/T790M/C797S blocker, induces cell death; promising for NSCLC research. IC50: 0.01 μM.</p>

<p>SL-176, a WIP1 inhibitor, when combined with GSK-J4, can induce cell cycle arrest and apoptosis (apoptosis), thereby inhibiting tumor growth both in vitro and in vivo.</p>

<p>MG-B-28, a BTLA-HVEM inhibitor, demonstrates an IC50 value of 906 nM. It promotes T cell activation dose-dependently by inhibiting the interaction between BTLA and HVEM.</p>