PD146176 (NSC168807) is a 15-Lipoxygenase (15-LO) inhibitor, which inhibits rabbit reticulocyte 15-LO with a Ki of 197 nM. PD146176 (NSC168807) has a dramatic effect in reducing atherogenesis[1].
Glibenclamide(Glyburide) is a sulfonylurea compound that modulates insulin production. IC50 value:Target:Sulfonylureas bind to ATP-dependent K+ channels in beta cells of the pancreas, depolarizing them and stimulating the release of Ca2+, which in turn stimulates insulin production. Glibenclamide, a sulphonylurea oral hypoglycaemic agent is a widely used antagonist of cromakalim-activated K+ channels in smooth muscle. Binding of Gli to SUR produces the closure of KATP channels and the inhibition of their activity. Glibenclamide is widely used for treatment of type 2-diabetes and it has been signaled as antiproliferative in several tumor cell lines.
EB-42486 is a novel, potent, and highly selective G2019S-LRRK2 inhibitor (IC50 < 0.2 nM).
Azathramycin is an antibiotic.
KU-55933 is a potent ATM inhibitor with an IC50 and Ki of 12.9 and 2.2 nM, respectively, and is highly selective for ATM as compared to DNA-PK, PI3K/PI4K, ATR and mTOR.
LD-ATTEC4 (compound 4A) is a coupling compound that can bind to LC3, with a Kd of 0.39 μM for LC3B. LD-ATTEC4 can connect autophagosomes with lipid droplets, inducing autophagy to clear lipid droplets[1].
Telaglenastat (CB-839) hydrochloride is a first-in-class, selective, reversible and orally active glutaminase 1 (GLS1) inhibitor. Telaglenastat hydrochloride selectively inhibits GLS1 splice variants KGA (kidney-type glutaminase) and GAC (glutaminase C) compared to GLS2. The IC50s are 23 nM and 28 nM for endogenous glutaminase in mouse kidney and brain, respectively. Telaglenastat hydrochloride inudces autophagy and has antitumor activity[1].
Idarubicin hydrochloride is an anthracycline antileukemic drug. It inhibits the topoisomerase II interfering with the replication of DNA and RNA transcription.
Quercetin is a natural flavonoid which activates or inhibits the activities of a number of proteins. Quercetin can activate SIRT1 and inhibit PI3K with IC50s of 2.4 μM, 3.0 μM, 5.4 μM for PI3K γ, PI3K δ and PI3K β, respecti
Vorinostat is a potent and orally available inhibitor of HDAC1, HDAC2 and HDAC3 (Class I), HDAC7 (Class II) and HDAC11 (Class IV ), with ID50 values of 10 nM and 20 nM for HDAC1 and HDAC3, respectively.
Malvidin-3-O-arabinoside chloride ameliorates ethyl carbamate-induced oxidative damage by stimulating AMPK-mediated autophagy[1].
Felodipine-d5 is deuterium labeled Felodipine. Felodipine, a dihydropyridine, is a potent, vasoselective calcium channel antagonist. Felodipine lowers blood pressure (BP) by selective action on vascular smooth muscle, especially in the resistance vessels. Felodipine, an anti-hypertensive agent, induces autophagy. Felodipine can cross the blood-brain barrier[1][2][3].
Lithocholic acid-d4 (3α-Hydroxy-5β-cholanic acid-d4) is the deuterium labeled Lithocholic acid, which is a toxic secondary bile acid[1].
JH-XII-03-02 is a potent and selective LRRK2 PROTAC degrader. JH-XII-03-02 can be used for parkinson's Disease (PD)?research[1].
Acetyl-coenzyme A (Acetyl-CoA) is a membrane-impermeant central metabolic intermediate, participates in the TCA cycle and oxidative phosphorylation metabolism. Acetyl-coenzyme A, regulates various cellular mechanisms by providing (sole donor) acetyl groups to target amino acid residues for post-translational acetylation reactions of proteins. Acetyl Coenzyme A is also a key precursor of lipid synthesis[1][2][3][4].
Salbutamol Hemisulfate is a short-acting β2 adrenergic receptor agonistTarget: β2 Adrenergic ReceptorSalbutamol is a short-acting, selective beta2-adrenergic receptor agonist used in the treatment of asthma and COPD. All the effects of R,S-salbutamol on guinea-pig skeletal muscles are due to the activity of the R-enantiomer. Thus there is a common enantiomeric profile for the skeletal muscle and bronchorelaxant activity of the compound [1]. Short-term Salbutamol intake did appear to improve performance during intense submaximal exercise with concomitant increase in substrate availability and utilization, but the exact mechanisms involved need further investigation [2]. Short-term administration of salbutamol increases voluntary muscle strength in man. However, the magnitude and duration of this effect vary between muscle groups. This study implies that the beta 2-adrenoceptor agonists may be of therapeutic potential in altering skeletal muscle function in humans [3].
Olacaftor (VX-440, VX440) is a next-generation CFTR corrector, shows the potential to enhance the amount of CFTR protein at the cell’s surface and for treatment of cystic fibrosis. Fibrosis Phase 2 Clinical
Imipramine is an orally active tertiary amine tricyclic antidepressant. Imipramine is a Fascin1 inhibitor with antitumor activities. Imipramine stimulates U-87MG glioma cells autophagy and induces HL-60 cell apoptosis. Imipramine shows neuroprotective and immunomodulatory effects[1][2][3][4].
3HOI-BA-01 is a mammalian targeting effective rapamycin activation inhibitor.
Entinostat is an oral and selective class I HDAC inhibitor, with IC50s of 243 nM, 453 nM, and 248 nM for HDAC1, HDAC2, and HDAC3, respectively.
SU9516 is a potent CDK2 inhibitor, with an IC50 of 22 nM, and also shows inhibitory effects on CDK1 and CDK4, with IC50s of 40, 200 nM, respectively.
Paroxetine-d4 (hydrochloride) is deuterium labeled Paroxetine (hydrochloride). Paroxetine hydrochloride is a potent selective serotonin-reuptake inhibitor, commonly prescribed as an and has GRK2 inhibitory ability with IC50 of 14 μM. Paroxetine hydrochloride can be used for the research of depressive disorder[1][2][3].
Dienogest(STS-557) is a specific progesterone receptor agonist with potent oral endometrial activity and is used in the treatment of endometriosis. Target: progesterone receptor agonistDienogest is an orally active synthetic progesterone (or progestin). It is available for use as an oral contraceptive in combination with ethinylestradiol. It has antiandrogenic activity and as a result can improve androgenic symptoms. It is a non-ethinylated progestin which is structurally related to testosterone [1]. Complete sperm suppression was observed in rats sacrificed either 60 or 90 days after dienogest (DNG)+ testosterone undecanoate (TU) administration, for two injections at 45-day interval. The neutral α-glucosidase activity in these treated rats remained in the normal range. Germ cell loss due to apoptosis was frequently observed both after 60 or 90 days of combination treatment. Significant decline in serum gonadotropin and testosterone, both serum and intratesticular levels, were observed in the treated rats. Following stoppage of treatment (given at 45-day interval) after two (0 and 45 days) or three injections (0, 45 and 90 days), complete restoration of spermatogenesis was observed by 120 and 165 days, respectively [2].Clinical indications: Adenomyosis; EndometriosisFDA Approved Date: 1995 Toxicity: weight gain; increased blood pressure; breast tenderness and nausea
Pirarubicin is an anthracycline antibiotics, acts as a topoisomerase II inhibitor, and is a widely used for treatment of various cancers, in particular, solid tumors.
Physalin B, one of the major active steroidal constituents of Cape gooseberry, induces cell cycle arrest and triggers apoptosis in breast cancer cells through modulating p53-dependent apoptotic pathway. Physalin B inhibits the ubiquitin-proteasome pathway and induces incomplete autophagic response in human colon cancer cells in vitro[1][2].
ATG12-ATG3 inhibitor 1 (compound 189) is a potent inhibitor of autophage[1].
UNC2400 is a close analog of UNC1999 with >1,000-fold lower potency than UNC1999 as a negative control for cell-based studies[1][2].
Fenretinide is a synthetic retinoid deriverative, binding to the retinoic acid receptors (RAR) at concentrations necessary to induce cell death.
LD-ATTEC2, an intermediate, used for lipid metabolism-related diseases study[1].
RapaLink-1, the third-generation bivalent mTOR inhibitor, combines Rapamycin with MLN0128 (a second-generation mTOR kinase inhibitor) by an inert chemical linker. RapaLink-1 shows better efficacy than Rapamycin or mTOR kinase inhibitors (TORKi), potently blocking cancer-derived, activating mutants of mTOR. RapaLink-1 can cross the blood-brain barrier. RapaLink-1 binding to FKBP12 results in targeted and durable inhibition of mTORC1. Anticancer activity[1][2].