Adenosine-13C5 is the 13C labeled Adenosine[1]. Adenosine (Adenine riboside), a ubiquitous endogenous autacoid, acts through the enrollment of four G protein-coupled receptors: A1, A2A, A2B, and A3. Adenosine affects almost all aspects of cellular physiology, including neuronal activity, vascular function, platelet aggregation, and blood cell regulation[2][3].
AZD5582 is a novel class of dimeric Smac mimetics as potent IAP antagonist; binds potently to the BIR3 domains of cIAP1, cIAP2, and XIAP (IC50 = 15, 21, and 15 nM, respectively). IC50 value: 15/21/15 nM (cIAP1/cIAP2/XIAP) [1]Target: IAPs inhibitorAZD5582 causes cIAP1 degradation and induces apoptosis in the MDA-MB-231 breast cancer cell line at subnanomolar concentrations in vitro. When administered intravenously to MDA-MB-231 xenograft-bearing mice, AZD5582 results in cIAP1 degradation and caspase-3 cleavage within tumor cells and causes substantial tumor regressions following two weekly doses of 3.0 mg/kg. Antiproliferative effects are observed with AZD5582 in only a small subset of the over 200 cancer cell lines examined, consistent with other published IAP inhibitors [1]. AZD5582 significantly enhanced apoptosis induced by the death receptor (DR) agonist tumour necrosis factor-related apoptosis-inducing ligand (TRAIL). Importantly, killing by TRAIL plus AZD5582 was independent of adverse prognostic features including TP53 deletion which is strongly associated with chemoresistance in CLL [2].
L-Glutamine-13C5,d5,15N2 (L-Glutamic acid 5-amide-13C5,d5,15N2) is the deuterium, 13C-, and 15-labeled L-Glutamine. L-Glutamine (L-Glutamic acid 5-amide) is a non-essential amino acid present abundantly throughout the body and involved in many metabolic processes. L-Glutamine provides a source of carbons for oxidation in some cells[1][2].
Tipiracil is a thymidine phosphorylase (TPase) inhibitor.
3-O-Acetyloleanolic acid (3AOA), an oleanolic acid derivative isolated from the seeds of Vigna sinensis K., induces in cancer and also exhibits anti-angiogenesis activity[1].
BTdCPU is a potent heme-regulated eIF2α kinase (HRI) activator. BTdCPU promotes eIF2α phosphorylation and induced apoptosis in resistant cell[1].
Kahweol is one of the consituents of the coffee from Coffea Arabica with anti-inflammatory anti-angiogenic, and anti-cancerous activities. Kahweol inhibits adipogenesis and increase glucose uptake by AMP-activated protein kinase (AMPK) activation. Kahweol induces apoptosis.
Tebufenozide-d9 is the deuterium labeled Tebufenozide[1]. Tebufenozide is a nonsteroidal ecdysone agonist used to control pest. Tebufenozide has cytotoxic and induces apoptosis in HeLa and insect Tn5B1-4 cells[2][3].
28-Deoxonimbolide is a nimbin (HY-N3187) type limonoid, that can be isolated from Azadirachta indica seed extracts. 28-Deoxonimbolide shows anticancer activity. 28-Deoxonimbolide induces apoptotic cell death in HL60 cells via both the mitochondrial- and the death receptor-mediated pathways[1].
HLI373 is an efficacious Hdm2 inhibitor. HLI373 inhibits the ubiquitin ligase activity of Hdm2. HLI373 is effective in inducing apoptosis of several tumor cells that are sensitive to DNA-damaging agents[1]. Antimalarial activity[2].
MS177 (MS-177) is a potent and selective EZH2 degarder (PROTAC) based on EZH2 inhibitor C24 with CRBN ligand pomalidomide with DC50 of 0.2 uM in EOL-1 cells.MS177 effectively degraded cellular EZH2-PRC2, suppressed global H3K27me3 in leukaemia cells.MS177 exhibited half-maximal degradation concentration (DC50) values of 0.2 ± 0.1 μM and 1.5 ± 0.2 μM, and maximum degradation (Dmax) values of 82% and 68%, respectively, in EOL-1 and MV4;11 cells.MS177 efficiently suppresses EZH2-PRC2 functions, also efficiently induces Myc degradation in cancer cells, suppresses EZH2-PRC2 functions.MS177 efficiently induces leukaemia cell growth inhibition, apoptosis and cell cycle progression arrest, which is more effective than EZH2 inhibitors. MS177 (i.p. injection, 50-1 g/kg) represses AML growth without apparent toxicity in PDX models.
Procyanidin C1 is a natural polyphenol, causes DNA damage, cell cycle arrest, and induces apoptosis. Procyanidin C1 decreases the level of Bcl-2, but enhances BAX, caspase 3 and 9 expression in cancer cells[1].
Mytoxin B is an ADC cytotoxin. Mytoxin B is a satratoxin-type trichothecene macrolide and is similar to the effect of LY294002 (HY-10108). Mytoxin B induces cell apoptosis via PI3K/Akt pathway[1].
Bacopaside II, an extract from the medicinal herb Bacopa monnieri, blocks the Aquaporin-1 (AQP1) water channel and impairs migration of cells that express AQP1. Bacopaside II induces cell cycle arrest and apoptosis[1][2].
Neoxanthin is a major xanthophyll carotenoid and a precursor of the plant hormone abscisic acid in dark green leafy vegetables. Neoxanthin is a potent antioxidant and light-harvesting pigment. Neoxanthin induces apoptosis and has anticancer actions[1][2].
Salvigenin is a natural polyphenolic compound, with neuroprotective effect. Salvigenin has antitumor cytotoxic and immunomodulatory properties[1][2].
Tomentosin is a antiphlogistic sesquiterpene lactone that can be isolated from Inula falconeri.Tomentosin induces Apoptosis and inhibits proliferation, migration and invasion of pancreatic cancer cells[1].
SHP2-IN-8 is a highly potent, selective, and cellularly active allosteric SHP2 inhibitor with IC50 value of 23 nM and Ki of 22 nM. SHP2-IN-8 is reversible and noncompetitive. SHP2-IN-8 causes a significant thermal shift with the ΔTm of 7.01 ℃. SHP2-IN-8 induces the apoptosis and inhibits the phosphorylation of AKT in Hela cells[1].
SU11652 is a potent receptor tyrosine kinase (RTK) inhibitor. SU11652 also inhibits several members of the split kinase family of RTKs, including VEGFR, FGFR, PDGFR, and Kit. SU11652 can be uesd for spontaneous cancers expressing Kit mutations research[1].
Z-Ala-Ala-Asp-CMK (Z-AAD-CMK) is a selective granzyme B inhibitor[1].
Anticancer agent 120 (compound 21) is an N-acylated ciprofloxacin derivative, which has certain antibacterial activity and induces ROS to promote cancer cell apoptosis[1].
IDO1/TDO-IN-1 (30) is a potent dual IDO1 (uncompetitive, Ki of 0.23 μM) and TDO (competitive, Ki of 0.73 μM) inhibitor. IDO1/TDO-IN-1 (30) significantly promotes cell apoptosis through the potential mitochondria-mediated Bcl-2/Bax pathway[1].
Astragaloside A is one of the major active constituents of Astragalus membranaceus in Traditional Chinese Medicine; has been widely used to treat ischemic diseases.IC50 value: Target: in vitro: AS-IV treatment promotes umbilical vein endothelial cells (HUVEC) proliferation, migration, and tube formation. AS-IV treatment also activates JAK2/STAT3 and ERK1/2 signaling pathways, and up-regulates endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production [1]. Administration of astragaloside IV (16, 32, and 64 μM) 1 h prior to lipopolysaccharide stimulation dose-dependently attenuated cardiac hypertrophy induced by lipopolysaccharide. Further studies demonstrated that astragaloside IV inhibited the increment of the resting intracellular free Ca2+, and its effect was similar to verapamil [2]. ASI could inhibit cells apoptosis induced by high glucose (25mmol/L) in dose-dependent and time-dependent manners. ASI also inhibited high glucose-induced expression of TGF-β1 and activation of p38 MAPK pathway at the protein level. Furthermore, ASI increased HGF production in human tubular epithelial cells [3].in vivo: the growth of tumor was suppressed by AS-IV treatment in vivo. AS-IV also could down-regulate regulatory T cells (Tregs) and up-regulate cytotoxic T lymphocytes (CTLs) in vivo and in vitro[4]. As an in vivo model, mice subjected to unilateral ureteral obstruction (UUO) were administered AS-IV (20 mg/kg) by intraperitoneal injection for 7 days. AS-IV significantly alleviated renal mass loss and reduced the expression of α-smooth muscle actin, fibronectin, and collagen IV both in vitro and in vivo [5].
BC-1258, an F-box/LRR-repeat protein 2 (FBXL2) activator, can stabilize and upregulate FBXL2 levels. BC-1258 induces apoptosis of tumorigenic cells, and profoundly inhibits tumor formation in mice[1].
AZA1 is a potent dual inhibitor of Rac1 and Cdc42. AZA1 induces prostate cancer cells apoptosis and inhibits prostate cancer cells proliferation, migration and invasion[1][2].
Neochamaejasmine A is a biflavonoid that can be isolated from the roots of Stellera chamaejasme L.. Neochamaejasmine A inhibits proliferation, induces cell cycle arrest and Apoptosis in tumor cells. Neochamaejasmine A can be used in the research of cancers such as prostate cancer, hepatoma cancer[1][2].
3,6-Dihydroxyflavone is an anti-cancer agent. 3,6-Dihydroxyflavone dose- and time-dependently decreases cell viability and induces apoptosis by activating caspase cascade, cleaving poly (ADP-ribose) polymerase (PARP). 3,6-Dihydroxyflavone increases intracellular oxidative stress and lipid peroxidation[1].
SKLB0565 is a potent tubulin inhibitor. SKLB0565 shows significant anti-proliferative activity against CRC (colorectal carcinoma) cell lines, with IC50 values ranging from 0.012 μM to 0.081 μM. SKLB0565 causes G2/M phase arrest and mitochondria-mediated intrinsic apoptosis. SKLB0565 inhibits cell migration and disrupted the tube formation of HUVECs[1].
BTM-3566 is an OMA1 activator. BTM-3566 activates the mitochondrial stress response. BTM-3566 induces apoptosis in diffuse large B-cell lymphomas (DLBCL) cell lines[1][2].
Trabectedin (Ecteinascidin-743 or ET-743) is a novel antitumour agent of marine origin with potent antitumour activity both in vitro and in vivo.IC50 Value: 0.1-3.7 nM (breast cancer cell lines) [1]Target: Apoptosis inducer; Anticancerin vitro: Trabectedin induced cytotoxicity and apoptosis in both breast cancer cells in a time and concentration-dependent manner. The expression levels of the death receptor pathway molecules, TRAIL-R1/DR4, TRAIL-R2/DR5, FAS/TNFRSF6, TNF RI/TNFRSF1A, and FADD were significantly increased by 2.6-, 3.1-, 1.7-, 11.2- and 4.0-fold by trabectedin treatment in MCF-7 cells. However, in MDA-MB-453 cells, the mitochondrial pathway related pro-apoptotic proteins Bax, Bad, Cytochrome c, Smac/DIABLO, and Cleaved Caspase-3 expressions were induced by 4.2-, 3.6-, 4.8-, 4.5-, and 4.4-fold, and the expression levels of anti-apoptotic proteins Bcl-2 and Bcl-XL were reduced by 4.8- and 5.2-fold in MDA-MB-453 cells [2]. In vitro treatment with noncytotoxic concentrations of trabectedin selectively inhibited the production of CCL2, CXCL8, IL-6, VEGF, and PTX3 by MLS primary tumor cultures and/or cell lines [3].in vivo: A xenograft mouse model of human MLS showed marked reduction of CCL2, CXCL8, CD68+ infiltrating macrophages, CD31+ tumor vessels, and partial decrease of PTX3 after trabectedin treatment [3]. The MTD of trabectedin was 700 microg/m(2) due to dose-limiting neutropaenia and the RDs in the previously treated/untreated patients were 500 and 600 microg/m(2), respectively. Most common toxicities were nausea/vomiting (67%), asthenia/fatigue (55%) and reversible ASAT/ALAT elevation (51%) [4]. Toxicity: Most common toxicities were nausea/vomiting (67%), asthenia/fatigue (55%) and reversible ASAT/ALAT elevation (51%) [4].Clinical trial: A Study to Assess the Potential Effects of Rifampin on the Pharmacokinetics of Trabectedin in Patients With Advanced Malignancies. Phase 1/2