Asp-AMS, an analogue of aspartyl-adenylate, is an aspartyl-tRNA synthetase inhibitor and also a strong competitive inhibitor of the mitochondrial enzyme.
Probucol is an anti-hyperlipidemic drug by lowering the level of cholesterol in the bloodstream by increasing the rate of LDL catabolism.Target: OthersProbucol is a drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. Probucol inhibited cholesterol efflux up to 80% in J774 macrophages expressing ABCA1. probucol is an effective inhibitor of ABCA1-mediated cholesterol efflux without influencing scavenger receptor class B type I-mediated efflux. The inhibition of ABCA1 translocation to the plasma membrane may in part explain the reported in vivo high-density lipoprotein-lowering action of probucol [1].
L-Leucine-d7 is the deuterium labeled L-Leucine. L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway[1].
UK-157147 is a substrate for UDP-glucuronosyltransferases (UGT1A1) with a Km value of 105 μM.
Probucol Disuccinate is a derivative of Probucol, a lipid-regulating agent and can reduce LDL-cholesterol levels[1].
Enclomiphene ((E)-Clomiphene) is a potent and orally active non-steroidal estrogen receptor antagonist, with antioestrogenic property. Enclomiphene can be used for the research of ovarian dysfunction, testosterone deficiency, male hypogonadism and type 2 diabetes[1].
TfR-T12 is a BBB-penetrated transferrin receptor (TfR) binding peptide, displaying a binding affinity in the nM range[1][2].
HM30181 is a potent and selective inhibitor of P-glycoprotein.
Cinnamtannin A2, a tetrameric procyanidin, can increases GLP-1 and insulin secretion in mice. Cinnamtannin A2 could upregulate the expression of corticotrophin releasing hormone. Cinnamtannin A2 exhibits antioxidant, anti-diabetic and nephroprotective effect[1][2].
Amylin (8-37), rat is a truncated analog of native Amylin that selectively inhibits insulin-related glucose uptake and glycogen deposition in muscle tissue. Amylin (8-37), rat is a weak amylin receptor (AMY) antagonist.
Tofogliflozin(CSG-452) hydrate is a potent and highly specific sodium/glucose cotransporter 2(SGLT2) inhibitor with Ki values of 2.9, 14.9, and 6.4 nM for human, rat, and mouse SGLT2.IC50 value: 2.9/14.9/6.4 nM(human/rat/mouse SGLT2) [1]Target: SGLT2 inhibitorin vitro: Tofogliflozin competitively inhibited SGLT2 in cells overexpressing SGLT2, and K(i) values for human, rat, and mouse SGLT2 inhibition were 2.9, 14.9, and 6.4 nM, respectively. The selectivity of tofogliflozin toward human SGLT2 versus human SGLT1, SGLT6, and sodium/myo-inositol transporter 1 was the highest among the tested SGLT2 inhibitors under clinical development [1]. tofogliflozin was catalyzed to the primary hydroxylated derivative (M4) by CYP2C18, CYP4A11 and CYP4F3B, then M4 was oxidized to M1. 3. Tofogliflozin had no induction potential on CYP1A2 and CYP3A4 [4].in vivo: A single oral gavage of tofogliflozin increased renal glucose clearance and lowered the blood glucose level in Zucker diabetic fatty rats. Tofogliflozin also improved postprandial glucose excursion in a meal tolerance test with GK rats. In db/db mice, 4-week tofogliflozin treatment reduced glycated hemoglobin and improved glucose tolerance in the oral glucose tolerance test 4 days after the final administration [1]. Tofogliflozin (400 ng/ml) induced UGE of about 2 mg/kg per min and increased EGP by 1-2 mg/kg per min, resulting in PG in the normal range [2]. Tofogliflozin suppressed plasma glucose and glycated Hb and preserved pancreatic beta-cell mass and plasma insulin levels. No improvement of glycaemic conditions or insulin level was observed with losartan treatment [3].
Lumasiran sodium, an investigational RNA interference (RNAi) therapeutic agent, reduces hepatic oxalate production by targeting glycolate oxidase. Lumasiran sodium reduces urinary oxalate excretion, the cause of progressive kidney failure in primary hyperoxaluria type 1 (PH1) [1][2].
H2-003 is a selective inhibitor of diacylglycerol acyltransferase 2 (DGAT2).
Forsythoside F (Arenarioside) is a xanthine oxidase inhibitor and possesses antihyperuricemic effects in vivo[1].
Gastric Inhibitory Polypeptide (6-30) amide (human) is an incretin hormone. Gastric Inhibitory Polypeptide (6-30) amide (human) can be used for the research of diabete[1].
Stearoyl-L-carnitine chloride is an endogenous long-chain acylcarnitine. Stearoyl-L-carnitine chloride is a less potent inhibitor of GlyT2. Stearoyl-L-carnitine chloride inhibits glycine responses by 16.8% at concentrations up 3 μM[1][2].
Acarbose sulfate is an inhibitor of alpha glucosidase, an anti-diabetic drug.
Xenin is a 25-amino acid peptide initially isolated from human gastric mucosa. Xenin is a gut hormone that can reduce food intake.
GSK1104252A is a potent and selective GPR119 agonist. GSK1104252A can be used for type 2 diabetes research[1].
MK-0493 is a potent, orally active and selective agonist of the melanocortin receptor 4 (MC4R), demonstrating significant reductions in energy intake[1].
L-Ornithine Hydrochloride is a free amino acid that plays a central role in the urea cycle and is also important for the disposal of excess nitrogen.
Estrogen receptor-IN-1 (compound 16) is a potent estrogen receptor (ER) inhibitor with IC50s of 13, 5µM for ERα and Erβ, respectively[1].
5'-Phosphoguanylyl-(3',5')-guanosine (pGpG) is an intermediate molecule produced by the pathway for enzymatic cyclic diguanylate (c-di-GMP) degradation. 5'-Phosphoguanylyl-(3',5')-guanosine can be used to detect the metabolism of nucleic acids[1][2].
As an aldose reductase (ALR2) inhibitor, the compound is used to enhance the combination of inhibitory excitability and antioxidant capacity to delay the progress of diabetes complications.
α-Homonojirimycin is a potent α-glucosidase inhibitor[1].
YM543 free base is a potent and orally active sodium-glucose cotransporter (SGLT) 2 inhibitor. YM543 free base reduces blood glucose levels. YM543 free base can be used in research of diabetes[1][2].
Velaglucerase alfa is produced through gene activation technology and is identical to wild-type enzyme. Velaglucerase alfa targets accumulated glucocerebroside primarily within the lysosome of the macrophages in the affected organs and systems. Velaglucerase alfa is an enzyme replacement therapy (ERT) for type 1 Gaucher disease (GD)[1].
D-Alanyl-L-leucine (D-Ala-Leu) is a dipeptide that acts as a source donor of L-Leucine (HY-N0486)[1].
(±)-SLV319 is the racemate of SLV319. SLV319 is a potent and selective cannabinoid-1 (CB-1) receptor antagonist with an IC50 of 22 nM.