FGFR-IN-8 (Compound 17a) is a highly potent and orally active panFGFR inhibitor against wild-type and mutant FGFRs. FGFR-IN-8 shows inhibition with IC50 values of <0.5, 189.1, <0.5, 22.6, <0.5 and 7.30 nM against FGFR1, V564F-FGFR2, N549H-FGFR2, V555M-FGFR3, FGFR3 and FGFR4, respectively. GFR-IN-8 induces cancer cell apoptosis and shows anticancer activities[1].
Verbenalin is Verbena glycoside, with anti-inflammatory, anti-fungal anti-virus activities. Verbenalin has a good effect on prostatitis. Verbenalin can reduce cerebral ischemia-reperfusion injury[1][2].
HI5 is a potent tublin and IDO inhibitor, with an IC50 value of 70 nM in HeLa cells. HI5 inhibit IDO expression and decrease kynurenine production, leading to stimulating T cells activation and proliferation. HI5 can inhibit tubulin polymerization and cell migration, cause G2/M phase arrest, and induce apoptosis via the mitochondrial dependent apoptosis pathway and cause reactive oxidative stress generation in HeLa cells. HI5 can be used for researching anticancer[1].
Cimiside E (25-Anhydrocimigenol xyloside) is a triterpene xyloside, Cimiside E possesses apoptotic action on gastric cancer cells, with an IC50 value of 14.58 μM. Cimiside E induces cell cycle arrest at G2/M phase, and mediates apoptosis through the induction of the Caspase cascade for both the extrinsic and intrinsic pathways[1][2].
L-Glutamine-13C5,15N2 (L-Glutamic acid 5-amide-13C5,15N2) is the 13C- and 15N-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].
Thalidomide D4 is a deuterium labeled Thalidomide. Thalidomide is initially promoted as a sedative, inhibits cereblon (CRBN), a part of the cullin-4 E3 ubiquitin ligase complex CUL4-RBX1-DDB1, with a Kd of ~250 nM, and has immunomodulatory, anti-inflammatory and anti-angiogenic cancer properties[1][2].
CDDO-3P-Im is an analogue of CDDO-Imidazolide with chemopreventive effect. CDDO-3P-Im can reduce the size and the severity of the lung tumors in mouse lung cancer model [1].
L-Glutamic acid monosodium hydrate is a nutritional additive and flavoring agent. L-Glutamic acid monosodium hydrate can reduce obesity and induce metabolic disorders associated with oxidative stress. L-Glutamic acid monosodium hydrate induces oxidative stress,DNA damage and apoptosis in the liver and brain tissues of mice[1][2].
S-Adenosyl-L-methionine (S-Adenosyl methionine) 1,4-butanedisulfonate is an orally active methyl group donor. S-Adenosyl-L-methionine 1,4-butanedisulfonate is a dietary supplement with potent antidepressant effects. S-Adenosyl-L-methionine 1,4-butanedisulfonate also has anti‑proliferative, pro‑apoptotic and anti‑metastatic roles in cancers. S-Adenosyl-L-methionine 1,4-butanedisulfonate has the potential for, cancer, liver disease and osteoarthritis research[1][2][3].
ABT-510 acetate is an anti-angiogenic TSP peptide (Thrombospondin-1 analogue) that induces apoptosis and inhibits ovarian tumour growth in an orthotopic, syngeneic model of epithelial ovarian cancer. ABT-510 acetate also reduces angiogenesis and inflammatory responses in a murine model of inflammatory bowel disease. ABT-510 acetate can be used in studies of cancer (particularly epithelial ovarian cancer) and inflammatory bowel disease (IBD)[1][2].
Pipernonaline is a piperine derivative with antiprostate cancer activity. Pipernonaline inhibits the proliferation of androgen-dependent/independent LNCaP/PC-3 prostate cells. Pipernonaline activates caspase-3 and promotes procaspase-3/PARP cleavage. Pipernonaline also mediates reactive oxygen species (ROS) production, increased intracellular Ca(2+), and mitochondrial membrane depolarization[1].
Gliotoxin is a secondary metabolite, the most abundant mycotoxin secreted by A. fumigatus, inhibits the phagocytosis of macrophages and the immune functions of other immune cells [1]. Gliotoxin inhibits inducible NF-κB activity by preventing IκB degradation, which consequently induces host-cell apoptosis[2]. Gliotoxin activates PKA and increases intracellular cAMP concentration; modulates actin cytoskeleton rearrangement to facilitate A. fumigatus internalization into lung epithelial cells[3].
BDA-366 is a potent Bcl2 antagonist (Ki = 3.3 nM), binding Bcl2-BH4 domain with high affinity and selectivity. BDA-366 induces conformational change in Bcl2 that abrogates its antiapoptotic function, converting it from a survival molecule to a cell death inducer. BDA-366 suppresses growth of lung cancer cells[1].
Vincristine-d3-ester (Leurocristine-d3-ester) sulfate is the deuterium labeled Vincristine sulfate. Vincristine sulfate is an antitumor vinca alkaloid which inhibits microtubule formation in mitotic spindle, resulting in an arrest of dividing cells at the metaphase stage. It binds to microtubule with a Ki of 85 nM[1].
5-Aminolevulinic acid-d2 (hydrochloride) is deuterium labeled 5-Aminolevulinic acid (hydrochloride).
Tauroursodeoxycholate-d4 is deuterium labeled Tauroursodeoxycholate. Tauroursodeoxycholate (Tauroursodeoxycholic acid) is an endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.
USP10 inhibitor Wu-5 (Wu-5) is a novel small molecule USP10 inhibitor inducing the degradation of FLT3-mutated protein, directly interacts and inactivates USP10, the deubiquitinase for FLT3-ITD in vitro (IC50=8.3 uM) and in FLT3-ITD-positive AML cells.Wu-5 selectively inhibited the viability of FLT3 inhibitor-sensitive (MV4-11, Molm13) and -resistant (MV4-11R) FLT3-ITD-positive AML cells with IC50 of 3.794, 5.056, and 8.386 uM, respectively.Wu-5 (1-10 μM) dose-dependently induced apoptosis of MV4-11, Molm13, and MV4-11R cells through the proteasome-mediated degradation of FLT3-ITD.Combined treatment of Wu-5 and crenolanib produced synergistic cell death in FLT3-ITD-positive cells via the reduction of both FLT3 and AMPKα proteins.
Antagonist G is a potent vasopressin antagonist. Antagonist G is also a weak antagonist of GRP and Bradykinin. Antagonist G induces AP-1 transcription and sensitizes cells to chemotherapy[1][2].
Sunitinib-d4 (SU 11248-d4) is the deuterium labeled Sunitinib. Sunitinib (SU 11248) is a multi-targeted receptor tyrosine kinase inhibitor with IC50s of 80 nM and 2 nM for VEGFR2 and PDGFRβ, respectively[1]. Sunitinib, an ATP-competitive inhibitor, effectively inhibits autophosphorylation of Ire1α by inhibiting autophosphorylation and consequent RNase activation[2].
Lepadin E is a significantly cytotoxic ferroptosis inducer that induces iron death through the classical p53-SLC7A11-GPX4 pathway. Lepadin E promoted p53 expression, decreases SLC7A11 and GPX4 levels, and leads to increased ROS and lipid peroxide production, and upregulated ACSL4 expression, thus causes cell death. Lepadin E has significant antitumor effect[1].
Topoisomerase II inhibitor 15 (compound 2g) is a Topoisomerase II inhibitor. Topoisomerase II inhibitor 15 potently is an apoptotic inducer with greater selectivity against head and neck tumors[1].
ABBV-167 is a phosphate prodrug of the BCL-2 inhibitor venetoclax.
Taurolidine is a broad-spectrum antimicrobial for the prevention of central venous catheter-related infections. Taurolidine has a direct and selective antineoplastic effect on brain tumor cells by the induction of apoptosis[1].
Cerivastatin sodium is a synthetic lipid-lowering agent and a highly potent, well-tolerated and orally active HMG-CoA reductase inhibitor, with a Ki of 1.3 nM/L. Cerivastatin sodium reduces low-density lipoprotein cholesterol levels. Cerivastatin sodium also inhibits proliferation and invasiveness of MDA-MB-231 cells, mainly by RhoA inhibition, and has anti-cancer effect[1][2].
SEL24-B489 (SEL24) is a potent, dual PIM and FLT3-ITD inhibitor with Kd of 2/2/3 nM for PIM1/2/3, Kd of 160/16 nM for FLT3-WT/FLT3-ITD, respectively; exhibits significantly broader on-target activity in AML cell lines (MV-4-11 GI50=20 nM) and primary AML blasts than selective FLT3-ITD or PIM inhibitors, decreases viability of AML cells with FLT3-TKD mutations associated with resistance to selective FLT3-ITD inhibitors; inhibits the growth of a broad panel of AML cell lines in xenograft models. Blood Cancer Phase 2 Clinical
Isoalantolactone is an apoptosis inducer, which also acts as an alkylating agent.
2-hydroxychalcone, a natural flavonoid, is a potent antioxidant, inhibiting lipid peroxidation. 2-Hydroxychalcone induces apoptosis by Bcl-2 downregulation. 2-Hydroxychalcone inhibits the activation of NF-kB[1][2][3].
cRIPGBM(chloride), an orally active, proapoptotic derivative. cRIPGBM can be generated from glioblastoma multiforme (GBM) cancer stem cells (CSCs). cRIPGBM(chloride) targets to receptor-interacting protein kinase 2 (RIPK2) to induce caspase 1-dependent apoptosis. cRIPGBM(chloride) suppresses the formation of RIPK2/TAK1 (prosurvival complex), and increases the formation of RIPK2/caspase 1 (proapoptotic complex). cRIPGBM(chloride) exerts potent anti-tumor activity in vivo in animal models[1].
COTI-2 is a small molecule candidate anti-cancer drug which can convert mutant p53 to wild-type conformation.