Hispidin, a PKC inhibitor and a phenolic compound from Phellinus linteus, has been shown to possess strong anti-oxidant, anti-cancer, anti-diabetic, and anti-dementia properties[1].
N-Acetylneuraminic acid-13C-2 is the 13C labeled N-Acetylneuraminic acid.
Rafigrelide is a platelet-lowering agent, and also has antithrombotic properties.
Peraquinsin is a MK2 activator. Peraquinsin can be used for the research of vascular disorder or endothelial barrier disorder. Peraquinsin also is an antihypertensive agent[1].
Mavacamten-d5 (MYK461-d5; SAR439152-d5) is deuterium labeled Mavacamten (HY-109037). Mavacamten (MYK461) is an orally active modulator of cardiac myosin, with IC50s of 490, 711 nM for bovine cardiac and human cardiac, respectively.
AZD4694, a fluorinated β-amyloid (Aβ) plaque neuroimaging PET radioligand, shows high affinity for Aβ fibrils (Kd = 2.3 nM)[1].
Losartan Carboxylic Acid (E-3174), an active carboxylic acid metabolite of Losartan, is an angiotensin II receptor type 1 (AT1) antagonist. The Ki values are 0.97, 0.57, 0.67 nM for rat AT1B/AT1A and human AT1, respectively. Losartan Carboxylic Acid blocks the angiotensin II-induced responses in vascular smoothmuscle cells (VSMC). Losartan Carboxylic Acid elevates plasma renin activities and reduces mean arterial pressure[1][2][3][4].
Diltiazem hydrochloride is a Ca2+ influx inhibitor (slow channel blocker or calcium antagonist).
(R)-(4′-Hydroxy)-5,7-dihydroxy-4-chromanone, a homoisoflavonoid, has antiangiogenic activity against human retinal microvascular endothelial cells[1].
Ambrisentan (BSF 208075) sodium is a selective and orally active ET type A receptor (ETAR) antagonist[1][2].
BMS-852927 is an LXRβ-selective agonist.
Arotinolol is a nonselective α/β-adrenergic receptor blocker and a vasodilating β-blocker. Arotinolol is an antihypertensive agent for the treatment of a variety of cardiovascular pathologies as well as non-cardiovascular diseases[1].
Teneligliptin D8 (MP-513 D8) a deuterium labeled Teneligliptin (MP-513). Teneligliptin is a potent, orally available, competitive, and long-lasting DPP-4 inhibitor[1].
Evatanepag (CP-533536) is an EP2 receptor selective prostaglandin E2 (PGE2) agonist that induces local bone formation with EC50 of 0.3 nM.IC50 value: 0.3 nM (EC50)Target PGE2in vitro: CP-533536 is a potent and selective EP2agonist. CP-533536 demonstrates the ability to heal fractures when administered locally as a single dose in rat models of fracture healing. CP-533536 demonstrates excellent in vitro potency against EP2 and selectivity against a broad panel of other targets.
Nitroprusside disodium dihydrate is a potent vasodilator working through releasing NO spontaneously in blood.Target: OthersNitroprusside disodium dihydrate is a potent vasodilator. Sodium nitroprusside has potent vasodilating effects in arterioles and venules. Sodium Nitroprusside breaks down in circulation to release nitric oxide (NO). NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP. The end result is vascular smooth muscle relaxation, which allow vessels to dilate [1]. Sodium nitroprusside decreases the proliferation of vascular smooth muscle cells [2]. Sodium nitroprusside (5 mg/kg) significantly reduces the intestinal ischemiareperfusion injury as a nitric oxide donor in rats [3].
PRL 3195 is a somatostatin receptor antagonist with Kis of 6, 17, 66, 1000 and 1000 nM for human somatostatin receptors (sst5, sst2, sst3, sst1 and sst4, respectively)[1].
Efonidipine Hcl (NZ-105) is a dual T-type and L-type calcium channel blocker (CCB).IC50 value: Target: calcium channel blockerin vitro: Efonidipine and nifedipine, but not other examined CCBs, also increased the N(6), 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP)-induced StAR mRNA, which reflects the action of adrenocorticotropic hormone, and efonidipine and R(-)-efonidipine enhanced the dbcAMP-induced DHEA-S production in NCI-H295R adrenocortical carcinoma cells [1]. I(Ca(T)) was blocked mainly by a tonic manner by nifedipine, by a use-dependent manner by mibefradil, and by a combination of both manners by efonidipine. IC50s of these Ca2+ channel antagonists to I(Ca(T)) and L-type Ca2+ channel current (I(Ca(L))) were 1.2 micromol/l and 0.14 nmol/l for nifedipine; 0.87 and 1.4 micromol/l for mibefradil, and 0.35 micromol/l and 1.8 nmol/l for efonidipine, respectively [4].in vivo: Twenty hypertensive patients on chronic hemodialysis were given efonidipine 20-60 mg twice daily and amlodipine 2.5-7.5 mg once daily for 12 weeks each in a random crossover manner. The average blood pressure was comparable between the efonidipine and amlodipine periods (151 + or - 15/77 + or - 8 versus 153 + or - 15/76 + or - 8 mmHg). The pulse rate did not change significantly during the administration periods [2]. In the UM-X7.1 group, EFO treatment significantly attenuated the decrease of LVEF without affecting blood pressure compared with the vehicle group. EFO treatment decreased heart rate (by approximately 10%) in both groups [3].
Fimasartan(BR-A-657) is a non-peptide angiotensin II receptor antagonist used for the treatment of hypertension and heart failure.IC50 value:Target: AT1 receptor antagonistin vitro: Fimasartan suppressed the expressions of inducible nitric oxide synthase (iNOS) by down-regulating its transcription, and subsequently inhibited the productions of nitric oxide (NO). In addition, fimasartan attenuated LPS-induced transcriptional and DNA-binding activities of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) [1]. BR-A-657 displaced [125I][Sar1-Ile8]angiotensin II (Ang II) from its specific binding sites to AT1 subtype receptors in membrane fractions of HEK-293 cells with an IC50 of 0.16 nM [2]. in vivo: After oral administration of 240 mg fimasartan, the mean area under the plasma concentration-time curve from time zero to infinity (AUC(0→∞)) was 2899.0 ng/ml/h in the older, which was significantly greater than in young subjects (1767.4 ng/ml/h; p = 0.03) [3]. Compared with atorvastatin alone, coadministration of fimasartan and atorvastatin increased the atorvastatin acid mean (95% confidence interval) maximum concentration (Cmax,ss) by 1.89-fold (1.49-2.39) and the area under the concentration curve (AUCτ,ss) by 1.19-fold (0.96-1.48). Fimasartan also increased the mean 2-hydroxy atorvastatin acid Cmax,ss and AUCτ,ss by 2.45-fold (1.80-3.35) and 1.42-fold (1.09-1.85), respectively [4].
5-HT2A antagonist 1 is a 5-HT2A antagonist extracted from patent US5728835A and JP 1007727. 5-HT2A antagonist 1 may be useful in treatment of gastrointestinal disorders circulatory disorders.
L-Aspartic acid-13C4 is the 13C-labeled L-Aspartic acid. L-Aspartic acid is is an amino acid, shown to be a suitable prodrug for colon-specific drug deliverly.
Irbesartan is a highly potent and specific angiotensin II type 1 (AT1) receptor antagonist with IC50 of 1.3 nM.Target: Angiotensin ReceptorIrbesartan treatment markedly induces the expression of the adipogenic marker gene adipose protein 2 (aP2) in 3T3-L1 cells in a concentration-dependent manner with EC50 of 3.5 μM and 3.3-fold induction at the concentration of 10 μM. Irbesartan (10 μM) markedly induces transcriptional activity of the peroxisome proliferator–activated receptor-γ (PPARγ) by 3.4-fold independent of its AT1 receptor blocking action. Pretreatment with Irbesartan (~10 μM) decreases angiotensin II-induced apoptosis in rat vascular smooth muscle cells by blocking angiotensin II internalization in a concentrationdependent manner. Oral administration of Irbesartan (1 mg/kg) reduces angiotensin II (AII)-induced hypertension, equipotent with losartan in conscious normotensive rats, markedly more active than losartan (10 mg/kg) in normotensive cynomolgus monkeys. Administration of Irbesartan (7 mg/kg/day) significantly prevents skeletal muscle apoptosis and muscle atrophy in rats with monocrotaline-induced congestive heart failure (CHF), which is involved with the decrease of TNFα level and attributed to AT1 receptor blocking.
Cycloolivil (Isoolivil) is a natural polyphenolic compound with a significant radical scavenging activity present in olive tree. Antioxidant and Antiaggregant effects[1].
S-(1,2-Dicarboxyethyl)glutathione is a peptide that inhibits blood coagulation and platelet aggregation[1].
ROCK1-IN-1 is a ROCK1 inhibitor with a Ki value of 540 nM. ROCK1-IN-1 can be used for the research of hypertension, glaucoma and erectile dysfunction[1].
Ned-K is a nicotinic acid adenine dinucleotide phosphate (NAADP) antagonist. Ned-K is effective at dampening simulated ischaemia and reperfusion (sIR)-induced Ca2+ oscillations in cardiomyocytes[1].
PD 123319 (ditrifluoroacetate) is a potent, selective AT2 angiotensin II receptor antagonist with IC50 of 34 nM.
Pimobendan is a selective inhibitor of PDE3 with IC50 of 0.32 μM.Target: PDE3Pimobendan exhibits selective inhibition of PDE III isolated from guinea pig cardiac muscle with IC50 of 0.32 uM compared to the inhibition of PDE I and PDE II (IC50s >30 μM). In human atrial cells, 100 μM pimobendan significantly increases the L-type calcium current (ICa(L)) (evoked by depolarization to +10 mV from a holding potential of -40 mV) by 250.4% with the half-maximal stimulation (EC50) of 1.13 μM. In rabbit atrial cells, Pimobendan increases ICa(L) at +10 mV by 67.4.%, which is significantly lower than that obtained in human atrial cells Pimobendan shows a beneficial effect on survival in the murine model of EMC virus-induced myocarditis. Administration of Pimobendan significantly increases the final survival rate from 33.6% (control) to 53.3% (0.1 mg/kg) or 66.7% (1 mg/kg). Pimobendan (1 mg/kg) also significantly reduces myocardial cellular infiltration, the level of intracardiac tumor necrosis factor (TNF)-α and interleukin (IL)-1β compared with the control group, which shows no effect on myocardial necrosis, heart weight and body weight. Pimobendan suppresses expression of the intracardiac iNOS gene , causing reduction of intracardiac NO production.
DHBP dibromide is an inhibitor for calcium release and a muscle relaxant.
(+)-Mepivacaine is a racemic isomer of Mepivacaine (HY-B0517), which has analgesic and vasoconstrictive activity. Mepivacaine is an amide type agent that temporarily causes local loss of consciousness. Mepivacaine binds to specific voltage-gated sodium channels on neuronal cell membranes, inhibiting sodium influx and membrane depolarization[1].
S107 hydrochloride is a RyR-selective 1,4-benzothiazepine derivative that stabilizes RyR2 channels by enhancing the binding affinity of calstabin2 to mutant and/or PKA-phosphorylated channels.