luciferase-in-1

Luciferase-IN-1 is a luciferase inhibitor that can be used to study bacterial and fungal infections.

Firefly luciferase-IN-1 is a 2-benzylidene tetrahydronaphthone derivative and can be used as a firefly luciferase inhibitor in kit.

KYN-101 is a potent, selective synthetic antagonist of aryl hydrocarbon receptor (AHR) with IC50 of 22 nM in human HepG2 DRE-luciferase reporter assay and 23 nM in murine Hepa1 Cyp-luc assay.KYN-101 reverses IDO/TDO-mediated tumor progression and improves the efficacy of PD-1 blockade in B16 IDO tumor-bearing mice, as well as CT26 colorectal cancer model expressing endogenous high levels of IDO.

N-(1-(3,4-Dihydroxyphenyl)propan-2-yl)oleamide binds to the cannabinoid 1 (CB1) receptor with a Ki value of 365 nM in a radioligand binding assay using rat brain homogenate. It has an EC50 value of 698 nM for the peroxisome proliferator-activated receptor α (PPARα) in a luciferase reporter assay and, in rats, it decreases food intake. It does not inhibit fatty acid amide hydrolase (FAAH).

20-HEPE is a metabolite of eicosapentaenoic acid that is formed via ω-oxidation of EPA by cytochrome P450 (CYP) ω-oxidases, including human CYP4F3B. It activates peroxisome proliferator-activated receptor α (PPARα) in COS-7 cells expressing a luciferase reporter when used at a concentration of 10 μM. 20-HEPE also activates murine transient receptor potential vanilloid receptor 1 (mTRPV1) in vitro but lacks antinociceptive activity in rats.

GW841819X is an analogue of (+)-JQ1 and a novel inhibitor of BET bromodomains. GW841819X was a single enantiomer but of undefined chirality at the 4-position of the benzodiazepine ring3. GW841819X and JQ1 were recently discovered that bind to the acetyl-lysine binding pocket of BET bromodomains with Kd ranges from 50 to 370 nM [1]. GW841819X bounded to both the individual BD1 and BD2 domains with affinities of 46 and 52.5 nM, respectively. GW841819X-Brd3 interaction was estimated to be around 70 nM4. GW841819X displayed activity in vivo against NUT-midline carcinoma, multiple myeloma, mixed-lineage leukemia, and acute myeloid leukemia1. It also potent induced the ApoA1 reporter gene with an EC50 of 440 nM. It had very little effect on LDL-R luciferase activity at the concentrations at which it induces ApoA1 expression, suggesting that the effect is indeed specific3. GW841819X competed directly with GATA1 site for BD1 binding and also specifically blocked the interaction between Brd3 and acetylated GATA14. Recent findings reported that GW841819X are chose as an interest compound to further develop into potential drugs against diseases including cancer, HIV infection and heart disease2.

MEISi-1 is a novel MEIS inhibitor (MEISi), significantly inhibiting MEIS-luciferase reporters in vitro and inducing murine (LSKCD34low cells) and human (CD34+, CD133+, and ALDHhi cells) HSC self-renewal ex vivo.

2-Bromo-1-decanal was synthesized as an affinity labeling probe for the aliphatic aldehyde site of Vibrio harveyi luciferase. In the presence of excess amounts of this probe, the inactivation of bacterial luciferase occurred following apparent first order

MD001 is a dual agonist of peroxisome proliferator-activated receptor α (PPARα) and PPARγ.1 It binds to PPARα and PPARγ (Kds = 9.55 and 0.14 μM, respectively) but does not bind to PPARβ/δ at concentrations up to 500 μM. It increases transcriptional activity of PPARα and PPARγ in a cell-based luciferase reporter assay when used at a concentration of 10 μM. MD001 (10 μM) increases expression of PPARα, PPARγ, and retinoid X receptor (RXR), as well as PPARα and PPARγ target genes, in HepG2 cells. It increases glucose consumption as well as expression of GLUT2 and GLUT4 in HepG2 and 3T3-L1 cells, respectively, in a concentration-dependent manner. MD001 (20 mg/kg) decreases levels of glucose, insulin, free fatty acids, triglycerides, LDL, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in blood and reduces the size and number of hepatic lipid droplets in diabetic db/db mice.References1. Kim, S.-H., Hong, S.H., Park, Y.-J., et al. MD001, a novel peroxisome proliferator-activated receptor α/γ agonist, improves glucose and lipid metabolism. Sci. Rep. 9(1), 1656 (2019). MD001 is a dual agonist of peroxisome proliferator-activated receptor α (PPARα) and PPARγ.1 It binds to PPARα and PPARγ (Kds = 9.55 and 0.14 μM, respectively) but does not bind to PPARβ/δ at concentrations up to 500 μM. It increases transcriptional activity of PPARα and PPARγ in a cell-based luciferase reporter assay when used at a concentration of 10 μM. MD001 (10 μM) increases expression of PPARα, PPARγ, and retinoid X receptor (RXR), as well as PPARα and PPARγ target genes, in HepG2 cells. It increases glucose consumption as well as expression of GLUT2 and GLUT4 in HepG2 and 3T3-L1 cells, respectively, in a concentration-dependent manner. MD001 (20 mg/kg) decreases levels of glucose, insulin, free fatty acids, triglycerides, LDL, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in blood and reduces the size and number of hepatic lipid droplets in diabetic db/db mice. References1. Kim, S.-H., Hong, S.H., Park, Y.-J., et al. MD001, a novel peroxisome proliferator-activated receptor α/γ agonist, improves glucose and lipid metabolism. Sci. Rep. 9(1), 1656 (2019).

AZ0108 is an orally bioavailable, potent PARP1,2,6 inhibitor that potently inhibits centrosome clustering and is suitable for in vivo efficacy and tolerability studies. AZ0108 has been utilized as in vitro tools and in vivo probes to investigate the biological consequences of inhibiting centrosome clustering through PARP enzymes. AZ0108 is more selective in its enzyme inhibition profile and effects on cellular pathways and phenotypes. Specifically, AZ0108 inhibits PARPs 1, 2, and 6 with approximately 100-fold selectivity against PARP3 and TNKS1. Consistent with this lack of potencytowards tankyrase, AZ0108 is not active in a DLD-1 Wnt luciferase reporter assay.