Trifluoperazine-d3 (dihydrochloride) is deuterium labeled Trifluoperazine (dihydrochloride). Trifluoperazine dihydrochloride, an antipsychotic agent, acts by blocking central dopamine receptors. Trifluoperazine dihydrochloride is a potent α1-adrenergic receptor antagonist. Trifluoperazine dihydrochloride is a potent NUPR1 inhibitor exerting anticancer activity. Trifluoperazine dihydrochloride is a calmodulin inhibitor, and also inhibits P-glycoprotein. Trifluoperazine dihydrochloride can be used for the research of schizophrenia. Trifluoperazine dihydrochloride acts as a reversible inhibitor of influenza virus morphogenesis[1][2][3][4][5].
PRE-084 hydrochloride is a high affinity, selective σ1 agonist, has an IC50 of 44 nM in the sigma receptor assay.IC50 value: 44 nMTarget: sigma receptorin vitro: PRE-084 has an IC50 of more than 100,000 nM for PCP receptors and an IC50 higher than 10,000 nM in a variety of other receptor systems. [1]in vivo: PRE-084 improves motor neuron survival and motor performance in wobbler mice. PRE-084 enhances BDNF-mediated trophic support.[2]
Blarcamesine (AVex-73;AE-37) is an orally bioavailable Sigma-1 receptor agonist and muscarinic receptor modulator, with anticonvulsant, anti-amnesic, neuroprotective and antidepressant properties. Blarcamesine ameliorates neurologic impairments in a mouse model of Rett syndrome[1].
Endomorphin 1 acetate, a high affinity, highly selective agonist of the μ-opioid receptor (Ki: 1.11 nM), displays reasonable affinities for kappa3 binding sites, with Ki value between 20 and 30 nM. Endomorphin 1 acetate has antinociceptive properties[1][2][4].
Telenzepine dihydrochloride is a selective and orally active muscarinic M1 receptor antagonist with a Ki of 0.94 nM. Telenzepine dihydrochloride inhibits gastric acid secretion and has antiulcer effects[1][2][3].
Ranatensin is a undecapeptide and a Bombesin Receptor angonist, can be isolated from amphibian skin, such as the frog, Rana pipiens. Ranatensin could maintain the dynamic balance of animal blood pressure, without cross-tachyphylaxis with Angiotensin amide (HY-P2212), Bradykinin (HY-P0206), or Norepinephrine (HY-13715)[1][2].
(R)-Viloxazine hydrochloride is a less active R-isomer of Viloxazine hydrochloride. Viloxazine hydrochloride is an effective antidepressant agent[1].
Xylometazoline is an α-adrenergic receptor agonist (Ki=0.05-1.7 μM). Xylometazoline can constrict nasal blood vessels and increase nasal airflow. Xylometazoline can be used in nose stuffiness and runny nose research[1][2].
Alizapride hydrochloride is a dopamine receptor antagonist with prokinetic and antiemetic effects which can also be used in the treatment of nausea and vomiting, including postoperative nausea and vomiting.
Azilsartan medoxomil(TAK 491) is an orally administered angiotensin II receptor type 1 antagonist with IC50 of 0.62 nM, which used in the treatment of adults with essential hypertension. IC50 Value: 0.62 nM [2]Target: AT1 receptorin vitro: In aortic endothelial cells, azilsartan inhibited cell proliferation at concentrations as low as 1 μmol/l, whereas valsartan showed little or no antiproliferative effects at concentrations below 10 μmol/l. Antiproliferative effects of azilsartan were also observed in cells lacking AT1 receptors[1].in vivo: Oral administration of 0.1-3 mg/kg olmesartan medoxomil reduced blood pressure; however, only the two highest doses significantly reduced blood pressure 24h after dosing. ED(25) values were 0.41 and 1.3 mg/kg for azilsartan medoxomil and olmesartan medoxomil, respectively [2]. Over a longer treatment period of 24 weeks, azilsartan medoxomil showed sustained BP-lowering efficacy, with the reduction in 24-hour mean SBP at week 24 significantly greater with azilsartan medoxomil 40 or 80 mg once daily than with valsartan 320 mg once daily. Mean reductions from baseline in mean clinic SBP and DBP as well as DBP by ABPM were also significantly greater with azilsartan medoxomil 40 or 80 mg once daily than with valsartan[3]. In 4 randomized controlled trials (3 published to date), azilsartan medoxomil/chlorthalidone 40 mg/12.5 mg and 40 mg/25 mg reduced blood pressure (BP) significantly more than comparators did, including an approximately 5-mm Hg greater BP reduction than olmesartan medoxomil/hydrochlorothiazide 40 mg/25 mg and azilsartan medoxomil/hydrochlorothiazide [4].
L-DOPA-2,5,6-d3 (Levodopa-2,5,6-d3) is the deuterium labeled L-DOPA. L-DOPA (Levodopa) is an orally active metabolic precursor of neurotransmitters dopamine. L-DOPA can cross the blood-brain barrier and is converted into dopamine in the brain[1][2][3].
Dopamine D2 receptor agonist-2 (compound 36) is a potent dopamine D2 receptor biased agonism ligand with an Ki value of 11.2 nM. Dopamine D2 receptor agonist-2 can be used to research antipsychosis[1].
Tarazepide is a potent and specific CCK-A receptor antagonist.
(S)-(-)-Propranolol hydrochloride is a β-adrenergic receptor antagonist with log Kd values of -8.16, -9.08, and -6.93 for β1, β2, and β3, respectively. (S)-(-)-Propranolol hydrochloride the active enantiomer of propranolol and can be s used for study of hypertension, pheochromocytoma, myocardial infarction, cardiac arrhythmias, angina pectoris, and hypertrophic cardiomyopathy[2].
UNC0642 is a potent and selective G9a/GLP inhibitor, with an IC50 of less than 2.5 nM.
Naloxegol (NKTR-118; AZ-13337019) is an opioid-receptor antagonist[1].
Sinomenine, an alkaloid extracted from Sinomenium acutum, is a blocker of the NF-κB activation[1]. Sinomenine also is an activator of μ-opioid receptor[2].
FSH receptor-binding inhibitor fragment(bi-10) is a potent FSH antagonist. FSH receptor-binding inhibitor fragment(bi-10) blocks the binding of FSH to FSHR, and alteres FSH action at the receptor level. FSH receptor-binding inhibitor fragment(bi-10) results in the suppression of ovulation and causes follicular atresia of mice. FSH receptor-binding inhibitor fragment(bi-10) has the potential for utilizing to restrain the carcinogenesis of ovarian cancer by down-regulating overexpression of FSHR and ERβ in the ovaries[1].
CYT-1010 hydrochloride is a mu-opioid receptor agonist extracted from patent WO2013173730A2, with EC50s of 13.1 nM and 0.0053 nM on beta-arrestin recruitment and inhibition of cAMP production, respectively[1].
KRAS G12C inhibitor 39 is a potent inhibitor of KRAS G12C. KRas is a highly attractable target of the pharmaceutical industry for cancer research. KRAS G12C inhibitor 39 has the potential for the research of KRAS G12C-mediated cancer (extracted from patent WO2019099524A1, compound 494)[1].
FAUC 213 is an orally active and highly selective dopamine D4 receptor complete antagonist with a Ki of 2.2 nM for hD4.4. FAUC 213 has less activity on D2 and D3 receptors (Kis of 3.4 μM, 5.3 μM for hD2, hD3, respectively). FAUC 213 can cross the blood-brain barrier (BBB). FAUC 213 exhibits atypical antipsychotic characteristic[1].
Naldemedine (S-297995) is an orally active, peripherally acting µ-opioid receptor antagonist. Naldemedine shows potent binding affinities (IC50s = 1.15, 1.11, and 1.5 nM, repectively) and antagonist activities (IC50s= 25.57, 7.09, 16.1 nM, repectively) for recombinant human μ-, δ-, and κ- opioid receptors. Naldemedine tempers opioid-induced constipation (OIC) without compromising opioid analgesia[1].
Acebutolol Hydrochloride is a β-adrenergic receptors antagonist used in the treatment of hypertension, angina pectoris and cardiac arrhythmias.Target: β-Adrenergic ReceptorAcebutolol is a beta blocker for the treatment of hypertension and arrhythmias. Acebutolol following single intravenous administration (10 mg/kg) to rat results in the plasma clearance of 61.9 mL/min/kg, the volume of distribution of 9.6 L/kg, and an elimination half-life of 1.8 hours. Acebutolol following single intravenous administration (50 mg/kg) to rat results in the plasma clearance of 46.5?mL/min/kg, the volume of distribution of 9.5?L/kg, and an elimination half-life of 2.3?hours [1]. Acebutolol (30 mg/kg) decreases cardiac output by 65% and 31% after 1 min and 10 min measurements, respectively, in Sprague-Dawley rats. Acebutolol (30 mg/kg) significantly reduces regional blood flow (RBF) in most organs either after 1 min or 10 min measurements when compare with the baseline values in Sprague-Dawley rats [2].
Phoenixin-14 (PNX-14) is one of the endogenous active isoform, and generates anxiolytic effect via the activation of the AHA GnRH system in mice. Phoenixin-14 inhibits ischemia/reperfusion-induced cytotoxicity in microglia[1][2].
Glucocorticoid receptor agonist-2 (compound 21) is an Glucocorticoid Receptor agonist with an IC50 value of 6.6 nM. Glucocorticoid receptor agonist-2 can be used to synthesize anti-inflammatory ADC molecules. Glucocorticoid receptor agonist-2 is an active reference of ABBV-3373[1].
VU0483605 is a potent and brain-penetrated mGlu1 receptor positive allosteric modulator (PAM). VU0483605 shows excellent mGlu1 PAM activity at both human and rat, with EC50 values of 390 and 356 nM, respectively[1].
Broxaterol (Z 1170) is the an agonist of β2 adrenergic receptor that affects the smooth muscle receptors in the body. Broxaterol plays an important role in respiratory disease[1].
Reparixin L-lysine salt is an allosteric inhibitor of chemokine receptor 1/2 (CXCR1/2) activation.
CXCR4 antagonist 1 is a potent CXCR4 antagonist. CXCR4 antagonist 1 has anti-HIV activity[1].
Silodosin (Rapaflo; KMD-3213) is an α1-adrenoceptor antagonist with high uroselectivity; In treatment of dysuria.IC50 Value:Target: Adrenergic Receptorin vitro: Silodosin potently inhibited 2-[2-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl]-alpha-tetralone binding to the cloned human alpha 1a-AR, with a Ki value of 0.036 nM, but had 583- and 56-fold lower potency at the alpha 1b- and alpha 1d-ARs, respectively. Silodosin inhibited norepinephrine-induced increases in intracellular Ca2+ concentrations in alpha 1a-AR-expressing Chinese hamster ovary cells with an IC50 of 0.32 nM but had a much weaker inhibitory effect on the alpha 1b- and alpha 1d-ARs.in vivo: Using pharmacologically well characterized native rat tissues [submaxillary gland (alpha 1A-AR-expressing tissue), liver (alpha 1B-AR-expressing tissue), and heart (mixed alpha 1A- and alpha 1B-AR-expressing tissue)], binding studies showed that inhibition curves for Silodosin in submaxillary gland and liver best fit a one-site model (with Ki values of 0.15 and 16 nM, respectively), whereas Silodosin had high and low affinity sites in heart membranes. Chloroethylclonidine treatment of rat heart membranes completely eliminated the low affinity sites for Silodosin. Furthermore, in human liver and prostate Silodosin could identify high and low affinity sites, the Ki values of which corresponded well to those for the cloned human alpha 1a- and alpha 1b-ARs, respectively. Moreover, the affinity of Silodosin was found to be approximately 10-fold higher at the cloned human alpha 1a-AR than at the cloned rat alpha 1a-AR.v