ABX-1431 is a highly potent, selective, and orally available, CNS-penetrant monoacylglycerol lipase (MAGL) inhibitor with an IC50 of 14 nM.
TM5007 is a poent and orally active inhibitor of plasminogen activator inhibitor-1 (PAI-1) with an IC50 of 29 μM. TM5007 enhance fibrinolysis activity and inhibits coagulation. TM5007 also prevents the fibrotic process initiated by bleomycin in mouse lung[1].
YM-08 (Compounds 7a) is a brain-penetrant inhibitors of SIRT2,with the IC50 of 19.9 μM. YM-08 also is inhibitor of Hsp70[1].
Vicenin 2 is an angiotensin-converting enzyme (ACE) inhibitor (IC50=43.83 μM) from the aerial parts of Desmodium styracifolium[1].
Dorzolamide(L671152; MK507) is an anti-glaucoma agent, which is a carbonic anhydrase inhibitor.Target: carbonic anhydrase (CA)Dorzolamide is a carbonic anhydrase inhibitor. It is an anti-glaucoma agent, and acts by decreasing the production of aqueous humour [1]. Glaucoma was induced in the right eye of adult Wistar rats by episcleral venous occlusion. One experimental group was administered dorzolamide 2%-timolol 0.5% combination eye drops, while the other experimental group was administered dorzolamide 2% eye drops. Control groups had surgery without drug administration. Drug application was initiated either 2 weeks before surgery (Group A), from the day of surgery (Group B), 2 weeks after surgery (Group C), or 4 weeks after surgery (Group D). RGCs were labeled by intratectal Fluorogold injections and counted from flat-mount preparations, and IOP was measured using Tonopen. Both dorzolamide-timolol combination and dorzolamide, when applied topically, significantly reduced IOP and improved RGC densities in experimental eyes when compared to control eyes. Earlier initiation, as well as longer duration of drug application, resulted in higher RGC densities [2].Clinical indications: Glaucoma; Ocular hypertensionFDA Approved Date: 1995Toxicity: Dizziness, headache, shortness of breath, slow heartbeat, severe asthma, cardiac arrest
Mutant IDH1-IN-6 is a potent, selective and orally active mutant isocitrate dehydrogenase (IDH) inhibitor with IC50s of 6.27 nM, 3.71 nM, 36.9 nM and 11.5 nM for IDH1 R132H, IDH1 R132C, IDH2 R140Q and IDH2 R172K mutant enzymes, respectively. Mutant IDH1-IN-6 is less active at inhibiting the IDH wild-type enzymes[1].
Flovagatran (TGN 255) is a potent and reversible thrombin inhibitor (Ki: 9 nM). Flovagatran can be used in the research of arterial and venous thrombosis[1].
Cabotegravir-d5 is deuterium labeled Cabotegravir.
EHNA hydrochloride is a specific inhibitor of adenosine deaminase, prevents dAdo degradation and increases mitochondrial dATP levels in fibroblasts[1].
2-TEDC is a potent inhibitor of 5-, 12-, and 15-lipoxygenase with IC50 values of 0.09 μM, 0.013 μM and 0.5 μM, respectively. 2-TEDC can be used for the research of atheroscrelosi[1].
CAY 10434 is a potent CYP4A hydroxylase inhibitor. CAY 10434 improves contractile response to angiotensin II with the maximal contractile response (Emax) 6764 mg[1].
Coblopasvir (KW-136) dihydrochloride is a pangenotypic non-structural protein 5A (NS5A) inhibitor. Coblopasvir dihydrochloride can be used for research of chronic hepatitis C virus infection[1].
Cyanidin 3-sambubioside chloride (Cyanidin-3-O-sambubioside chloride), a major anthocyanin, a natural colorant, and is a potent NO inhibitor. Cyanidin 3-sambubioside chloride is a H274Y mutation inhibitor, and inhibits influenza neuraminidase activity with an IC50 of 72 μM. Cyanidin 3-sambubioside chloride inhibits angiotensin-converting enzyme (ACE) activity and has antioxidant, anti-angiogenic and antiviral properties[1][2][3].
MAL3-101 is a Hsc70 modulator that inhibits Hsp70 ATPase activity, exhibits antiproliferative activity in breast cancer cells SK-BR-3 with IC50 of 27 uM; also exhibits antimyeloma effects on MM cell lines in vitro and in vivo in a xenograft plasmacytoma model, as well as on primary tumor cells and bone marrow endothelial cells from myeloma patients.
HIF-2α-IN-3, an allosteric inhibitor of hypoxia inducible factor-2α (HIF-2α), exhibits an IC50 of 0.4 µM and a KD of 1.1 µM. Anticancer agent[1].
CDP-840 (GR259653X) is a potent, selective and orally active phosphodiesterase IV (PDE IV) inhibitor. CDP-840 inhibits antigen-induced early and late phase bronchoconstriction in conscious squirrel monkeys[1].
Lavendustin B is an inhibitor of HIV-1 integrase interaction with LEDGF/p75 with an IC50 of 94.07 μM. Lavendustin B is an ATP-competitive GLUT1 inhibitor with a Ki of 15 µM. Lavendustin B is also a weak inhibitor of tyrosine kinases[1][2].
QH536 (Compound 29) is a potent HMGCR degrader with an EC50 of 0.22 μM. QH536 has no side-effect of inducing cholesterol accumulation in cells. QH536 shows anti-inflammatory and can be used for cardiovascular disease and nonalcoholic steatohepatitis research[1].
IDO-IN-14 is an IDO inhibitor with an IC50 value of 0.6928 nM.
Palovarotene is a nuclear retinoic acid receptor γ (RAR-γ) agonist.
KS106 is a potent ALDH inhibitor with IC50s of 334, 2137, 360 nM for ALDH1A1, ALDH2, and ALDH3A1, respectively. KS106 shows antiproliferative and anticancer effects with low low toxic.KS106 significantly increases ROS activity, lipid peroxidation and toxic aldehyde accumulation. KS106 induces apoptosis and cell cycle arrest at the G2/M phase[1].
Dimethylfraxetin is a Carbonic anhydrase inhibitor, with a Ki value of 0.0097 μM.
BI 224436 is a novel HIV-1 noncatalytic site integrase inhibitor with EC50 values of less than 15 nM against different HIV-1 laboratory strains.
STL5-T-0057 (compound 68) is an selective ALDH1 B1 inhibitor with an IC50 value of 30 nM. STL5-T-0057 inhibits cell growth of SW480 cells in adherent and spheroid conditions with IC50 values of 2.46 and 0.39 μM, respectively. STL5-T-0057 can be used for the research of cancer[1].
Linagliptin-d4 is deuterium labeled Linagliptin. Linagliptin is a highly potent, selective DPP-4 inhibitor with IC50 of 1 nM.
AZD-0284 is an inverse agonist of the nuclear receptor RORγ. In development for the treatment of plaque psoriasis vulgaris and respiratory tract disorders[1].
(3S,5R)-Rosuvastatin is the (3S,5R)-enantiomer of Rosuvastatin. Rosuvastatin is a competitive HMG-CoA reductase inhibitor with an IC50 of 11 nM[1]. Rosuvastatin potently blocks human ether-a-go-go related gene (hERG) current with an IC50 of 195 nM[2]. Rosuvastatin reduces the expression of the mature hERG and the interaction of heat shock protein 70 (Hsp70) with the hERG protein. Rosuvastatin is very effective in lowering low-density lipoprotein (LDL) cholesterol, triglycerides, and C-reactive protein levels[3].
Ovotransferrin (328-332) has a protective activity on the blood pressure by inhibiting the Angiotensin-Converting Enzyme (ACE), with the IC50 of 20 μM. Ovotransferrin (328-332) fragment has an activity against Cholinesterase (ChE), implicating in Alzheimer’s diseases[1][2].
Palmitic acid-13C is the 13C-labeled Palmitic acid. Palmitic acid is a long-chain saturated fatty acid commonly found in both animals and plants. Palmitic acid can induce the expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in in mouse granulosa cells[1][2].
Acetyl-11-Keto-β-Boswellic Acid (AKBA) is an active triterpenoid compound from the extract of Boswellia serrate; a novel Nrf2 activator.IC50 value:Target: Nrf2 activatorin vitro: AKBA significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE) [1]. AKBA significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell cycle in G1-phase and induction of apoptosis[3]. AKBA triggered significant lipolysis in 3T3-L1 adipocytes as shown by reduced neutral lipids in cytosol and increased free fatty acids in culture medium. Increased lipolysis by AKBA was accompanied by up-regulation of lipolytic enzymes, adipocyte triglyceride lipase (ATGL) and hormone sensitive lipase (HSL), and a decreased expression of lipid droplet stability regulator perilipin. In addition, AKBA treatment reduced phenotypic markers of mature adipocyte aP2, adiponectin and glut-4 in mature adipocytes [5].in vivo: AKBA significantly prevented the formation of intestinal adenomatous polyps without toxicity to mice. AKBA's activity both in the prevention of small intestinal and colonic polyps was more potently than aspirin. Histopathologic examination revealed that AKBA's effect, that is the reduction of polyp size and degree of dysplasia, was more prominent in larger sized polyps, especially those originating in colon [2]. AKBA administration in mice effectively delayed the growth of HT-29 xenografts without signs of toxicity. The activity of AKBA was more potent than that of aspirin [3]. AKBA exhibited anti-cancer activity in vitro and in vivo. With oral application in mice, AKBA significantly inhibited SGC-7901 and MKN-45 xenografts without toxicity [4].