N-Acetyl-Ser-Asp-Lys-Pro is a natural and specific substrate for the N-terminal site of ACE.
(S)-Lercanidipine D3 (hydrochloride) is a deuterium labeled Lercanidipine D3 hydrochloride. (S)-Lercanidipine hydrochloride is an antihypertensive agent[1].
TGP-377/421 (Targapre-miR-377/421) is a smalll molecule targets pre-miR-377 and inhibits its processing, binds to miR-377's Dicer processing site with Kd of 29 uM.TGP-377/421 inhibits the cellular biogenesis of miR-377 in HUVECs, reduced mature miR-377 levels in a dose-dependent fashion with IC50 of 5 uM, also inhibits miR-421.
Cinnarizine D8 is a deuterium labeled Cinnarizine. Cinnarizine is an antihistamine and a calcium channel blocker.
Acebutolol is an orally active β1 adrenergic receptor (β1AR) antagonist. Acebutolol is used for hypertension, angina pectoris and cardiac arrhythmias research[1][2][3].
Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist.
(±)-Equol is the racemate of equol. Equol is a metabolite of the soy isoflavones, daidzin and daidzein.
Arrhythmias-Targeting Compound 1 is used in the research of arrhythmias, extracted from patent WO 2001028992 A2.
Norverapamil is a calcium channel blocker， it is the main active metabolite of verapamil.In vitro: Norverapamil is similarly effective as verapamil at inhibiting isoniazid and rifampicin tolerance and killing of intracellular M. tuberculosis in the absence of other drugs. norverapamil, also inhibits macrophage-induced tolerance and achieves similar serum levels to verapamil.[1] Norverapamil (NOR) is the major metabolite and shows approximately 20% of the efficacy of VER with regard to the vasodilation effect, but shows no antiarrhythmic activity. [2] Verapamil and its major metabolite norverapamil were identified to be both mechanism-based inhibitors and substrates of CYP3A and reported to have non-linear pharmacokinetics in clinic. [3]
Takeda103A is a potent inhibitor of GRK2. G protein-coupled receptors (GPCRs) are central to many physiological processes. Takeda103A has the potential for the research of heart failure[1].
Novel upregulator of TRIB1 expression, leading to reprogramming of hepatic lipoprotein metabolism from lipogenesis to scavenging
Argatroban monohydrate is a direct, selective thrombin inhibitor.Target: ThrombinArgatroban may have a complementary effect for preventing thrombus formation without aggravating bleeding tendency because of its monotarget specificity to thrombin. Administration (0.5 to 2 micrograms/kg/min) of argatroban is a safe anticoagulant for left heart bypass in repairs of traumatic aortic rupture associated with multiple organ injuries [1]. Argatroban, as compared with heparin, appears to enhance reperfusion with TPA in patients with AMI, particularly in those patients with delayed presentation. The incidences of major bleeding and adverse clinical outcome were lower in the patients receiving argatroban [2].
Hydrochlorothiazid-13C,d2 is the 13C- and deuterium labeled. Hydrochlorothiazide (HCTZ), an orally active diuretic drug of the thiazide class, inhibits transforming TGF-β/Smad signaling pathway. Hydrochlorothiazide has direct vascular relaxant effects via opening of the calcium-activated potassium (KCA) channel. Hydrochlorothiazide improves cardiac function, reduces fibrosis and has antihypertensive effect[1][2][3].
Zerlasiran is an apolipoprotein A (ApoA) synthesis reducer[1].
NS5806, a potent potassium current activator, increases KV4.3/KChIP2 peak current amplitudes with an EC50 of 5.3 μM. NS5806 slows KV4.3 and KV4.2 current dacay in channel complexes containing KChIP2[1].
RXP470.1 (RXP-470) is a potent, selective MMP-12 inhibitor with a Ki of 0.2 nM against human MMP-12. RXP470.1 is 2 to 4 orders of magnitude less potent against other MMPs. RXP470.1 significantly reduces atherosclerotic plaque cross-sectional area in mouse. RXP470.1 results in less complex plaques with increased smooth muscle cell:macrophage ratio, less macrophage apoptosis, increased cap thickness, smaller necrotic cores, and decreased incidence of calcification[1].
TRV056 is a Gq-biased ligand of the angiotensin II receptor type 1 (AT1R). TRV056 is efficacious in stimulating cellular Gq-mediated signaling. TRV056 can be used to develop the Gq-biased AT1R agonists[1].
Ginsenoside Rd inhibits TNFα-induced NF-κB transcriptional activity with an IC50 of 12.05±0.82 μM in HepG2 cells. Ginsenoside Rd inhibits expression of COX-2 and iNOS mRNA. Ginsenoside Rd also inhibits Ca2+ influx. Ginsenoside Rd inhibits CYP2D6, CYP1A2, CYP3A4, and CYP2C9, with IC50s of 58.0±4.5 μM, 78.4±5.3 μM, 81.7±2.6 μM, and 85.1±9.1 μM, respectively.
Prazosin is an alpha-adrenergic blocker and is a sympatholytic drug used to treat high blood pressure and anxiety, PTSD, and panic disorder.Target: Adrenergic ReceptorPrazosin, is a sympatholytic drug used to treat high blood pressure and anxiety, PTSD, andpanic disorder. It is an alpha-adrenergic blocker that is specific for the alpha-1 receptors. These receptors are found on vascular smooth muscle, where they are responsible for the vasoconstrictive action of norepinephrine. They are also found throughout the central nervous system. As of 2013, prazosin is off-patent in the US, and the FDA has approved at least one generic manufacturer.In addition to its alpha-blocking activity, prazosin is an antagonist of the MT3 receptor (which is not present in humans), with selectivity for this receptor over the MT1 and MT2 receptors.Prazosin is orally active and has a minimal effect on cardiac function due to its alpha-1 receptor selectivity. However, when prazosin is initially started, heart rate and contractility go up in order to maintain the pre-treatment blood pressures because the body has reached homeostasis at its abnormally high blood pressure. The blood pressure lowering effect becomes apparent when prazosin is taken for longer periods of time. The heart rate and contractility go back down over time and blood pressure decreases.
Indecainide hydrochloride is a potent and orally active class I local anesthetic antiarrhythmic agent[1].
Gypenoside inhibits endothelial cell apoptosis in atherosclerosis by modulating mitochondria through PI3K/Akt/Bad pathway[1]. And Gypenoside possesses neuroprotective, anticancer, anti-oxidant, anti-inflammatory, anti-diabetic, and anti-
Benzthiazide is a long-acting diuretic[1] and a hypertension agent. Benzthiazide is an inhibitor of carbonic anhydrase 9 (CA9), with Kis of 8.0, 8.8 and 10 nM for CA9, CA2 and CA1, respectively. Benzthiazide also suppresses proliferation of cancer cells[2].
Cyclic ADP-ribose (cADPR) is a potent second messenger for calcium mobilization that is synthesized from NAD+ by a ADP-ribosyl cyclase. Cyclic ADP-ribose increases cytosolic calcium mainly by Ryanodine receptor-mediated release from endoplasmic reticulum and also by extracellular influx through the opening of TRPM2 channels[1].
Lanatoside B is a cardenolide that can be isolated from the leaves of Digitalis lanata[1].
BMS-309403 is a potent, selective and cell-permeable inhibitor of fatty acid binding protein 4 (FABP4) with a Ki of less than 2 nM.
Ilexsaponin B3 has significant hypocholesterolemic activity[1].
Etilefrine (3-[2-(ethylamino)-1-hydroxyethyl]phenol) is an α adrenergic agonist[2]. Etilefrine also is an AMPK activator[1]. Etilefrine can be used for the research of postural hypotension[3].
CYM50308 is a potent, selective and high affinity sphingosine-1-phosphate receptor 4 (S1P4-R) agonist with an EC50 of 56 nM. CYM50308 displays 37-fold more selective for S1P4-R than S1P5-R. CYM50308 has no activity at S1P1-R, S1P2-R and S1P3-R subtypes at concentrations up to 25 μM[1].
Angiotensinogen (1-13) (human) is a fragment of the renin substrate angiotensinogen. Angiotensinogen is naturally occurring substrate for renin and a precursor for all angiotensin peptides[1][2].
GlyH-101 is a cell-permeable glycinyl hydrazone compound that blocks CFTR with Ki of 1.4 uM.IC50 value: 1.4 uM (Ki, at +60 mV) [1]Target: CFTRin vitro: GlyH-101 reversibly inhibited CFTR Cl- conductance in <1 min. Whole-cell current measurements revealed voltage-dependent CFTR block by GlyH-101 with strong inward rectification, producing an increase in apparent inhibitory constant Ki from 1.4 microM at +60 mV to 5.6 microM at -60 mV. GlyH-101 inhibitory potency was independent of pH from 6.5-8.0, where it exists predominantly as a monovalent anion with solubility approximately 1 mM in water[1]. In HeLa cells, these events were associated with a decrease in the rate of oxygen consumption, with GlyH-101 demonstrating a higher potency than CFTR(inh)-172. The impact of CFTR inhibitors on inflammatory parameters was also tested in HeLa cells. CFTR(inh)-172, but not GlyH-101, induced nuclear translocation of nuclear factor-kappaB (NF-kappaB) [2]. GlyH-101 is a glycine hydrazide that has recently been shown to block CFTR channels but its effects on cardiomyocytes are unknown. Here the action of GlyH-101 on cardiac I(Cl.PKA) and on other ion currents has been established. Whole-cell patch-clamp recordings were made from rabbit isolated ventricular myocytes. GlyH-101 blocked I(Cl.PKA) in a concentration- and voltage-dependent fashion (IC(50) at +100 mV=0.3 ± 1.5 μM and at -100 mV=5.1 ± 1.3 μM) [3].in vivo: Topical GlyH-101 (10 microM) in mice rapidly and reversibly inhibited forskolin-induced hyperpolarization in nasal potential differences. In a closed-loop model of cholera, intraluminal GlyH-101 (2.5 microg) reduced by approximately 80% cholera toxin-induced intestinal fluid secretion [1].