Carbazochrome(AC-17) is an antihemorrhagic agent.Target: OthersCarbazochrome is an antihemorrhagic agent that will cease blood flow by causing the aggregation and adhesion of platelets in the blood to form a platelet plug, ceasing blood flow from an open wound. It is hoped that this drug can be used in the future for preventing excessive blood flow during surgical operations and the treatment of hemorrhoids. Carbazochrome interacts with α-adrenoreceptors on surface of platelets, which are coupled to Gq protein and initiate PLC IP3/DAG pathway to increase intracellular free calcium concentration with these subsequent actions. Activates PLA2 and induce arachidonic acid pathway to synthese endoperoxides (TxA2, thromboxane A2). Calcium binds to calmodulin which then binds and activates myosin light-chain kinase, that will enable the myosin crossbridge to bind to the actin filament and allow contraction to begin. This will change platelet's shape and induce release of serotonin, ADP, vWF (Von Willebrand factor), PAF (Platelet-activating factor) to promote further aggregation and adhesion. From Wikipedia.
Mavrilimumab (CAM 3001) is a monoclonal antibody that binds to the α subunit of the granulocyte-macrophage colony stimulating factor (GM-CSF) receptor and blocks intracellular signalling downstream of GM-CSF. GM-CSF might be a mediator of the hyperactive inflammatory response associated with respiratory failure and death[1].
C-Reactive Protein (CRP) 201-206 is the 201-206 fragment of C-Reactive Protein. C-Reactive Protein (CRP), the prototypic marker of inflammation, is a cardiovascular risk marker and may promote atherogenesis[1].
Bucindolol is a β1-adrenergic receptor blocker, with intrinsic sympathomimetic activity, used in the research of heart failure[1].
SR59230A hydrochloride is a potent, selective, and blood-brain barrier penetrating β3-adrenergic receptor antagonist[1] with IC50s of 40, 408, and 648 nM for β3, β1, and β2 receptors, respectively[2].
AGDV is the γ chain of fibrinogen. AGDV is critical for platelet aggregation[1][2].
Almokalant is a class III antiarrhythmic drug, acts as a potassium channel blocker, and inhibits a specific component (Ikr) of the time-dependent delayed rectifier K+ current.
Sodium formononetin-3'-sulfonate (Sul-F) is a water-sol. derivate of formononetin. IC50 value:Target: Research results showed that treatment with Sul-F significantly prevented the elevation of ST-segment level, decreased the contents of creatine kinase-MB, lactate dehydrogenase, alanine aminotransferase and cardiac troponin T in serum and reduced the myocardium necrosis scores. These findings indicate that Sul-F has a protective potential against myocardial infarction injury. A possible mechanism for the protective effect is the elevated expression of endogenous antioxidant defense enzymes degraded lipid peroxidn. products and improved energy metab. of cardiac mitochondrial, thus attenuating cardiocyte apoptosis. Other reaearch results showed that sodium formononetin-3'-sulfonate not only had favorable water, solubility but also had good lipid-lowering and liver-protection activities.
Vernakalant-d6 (hydrochloride) is deuterium labeled Vernakalant.
NF449 octasodium is a highly potent P2X1 receptor antagonist, with IC50s of 0.28, 0.69, and 120 nM for rP2X1, rP2X1+5, P2X2+3, respectively. NF449 octasodium is a Gsα-selective G Protein antagonist. NF449 octasodium suppresses the rate of GTP[γS] binding to Gsα-s, inhibits the stimulation of adenylyl cyclase activity, and blocks the coupling of β-adrenergic receptors to Gs[1][2].
Rentiapril racemate is the racemate of Rentiapril. Rentiapril is an angiotensin converting enzyme (ACE) inhibitor.
EXP3179 is an important intermediate aldehyde metabolite of Losartan. EXP3179 has no AT1-R–blocking activity, but potently inhibits the expression of endothelial cyclooxygenase (COX)-2. EXP3179 exerts potent anti-inflammatory actions[1].
NF864, a suramin analog, is a P2X1 receptor inhibitor.
Bunazosin is a potent and selective α1-adrenoceptor antagonist. Bunazosin can be used for antihypertensive and ocular hypotensive research[1].
Verapamil-d6 (CP-16533-1-d6) hydrochloride is the deuterium labled Verapamil (hydrochloride) (HY-A0064). Verapamil hydrochloride ((±)-Verapamil hydrochloride) is a calcium channel blocker and a potent and orally active first-generation P-glycoprotein (P-gp) inhibitor. Verapamil hydrochloride also inhibits CYP3A4. Verapamil hydrochloride has the potential for high blood pressure, heart arrhythmias and angina research[1][2][3].
BMS-986224 is a potent, selective and orally bioavailable APJ receptor agonist (Kd = 0.3 nM). BMS-986224 exhibits similar receptor binding and signaling profile to (Pyr1) apelin-13. BMS-986224 has the potential for the research of heart failure[1].
Imidapril-d3 hydrochloride (TA-6366-d3) is the deuterium labeled Imidapril hydrochloride. Imidapril hydrochloride (TA-6366) is the hydrochloride salt of Imidapril, an angiotensin-converting enzyme (ACE) inhibitor with antihypertensive activity[1][2].
Hydroxy Bosentan-d6 is deuterium labeled Hydroxy bosentan. Hydroxy bosentan (Ro 48-5033) is a primary metabolite of Bosentan (BOS) metabolized by the cytochrome P450 system in the liver. Ro 48-5033 assists BOS pharmacologically, retaining 10%-20% activities[1].
Xipamide-d6 is the deuterium labeled Xipamide. Xipamide is a sulfonamide-based diuretic. Xipamide is an antihypertensive agent able to selectively inhibit the anion exchanger (AE)[1][2].
Hispolon, a polyphenol, can be isolated from Phellinus linteus. Hispolon possesses anticancer, antidiabetic, antioxidant, antiviral, hepatoprotective, anti-diabetic, and anti-inflammatory activities[1].
SCH00013 is a cardiotonic agent that primarily acts via an increase in myofibrillar Ca++ sensitivity, have a significant Ca(2+)sensitizing effect at pH 7.2 to 7.4.In vitro: SCH00013 at 10-4 M increased the systolic cell shortening by 52% above the base-line value in association with an insignificant increase in the systolic fluorescence ratio by 15% above the control. [1]In vivo: The positive inotropic effects of 10?4 M SCH00013 on the dog and rabbit were 38% and 29% of the maximal response to isoproterenol. [1] CH00013 elicited a positive inotropic effect at more than 0.3 and 1 mg/kg, i.v. in normal and heart failure dogs. [2] SCH00013 elicits a positive inotropic effect mainly through an increase in myofilament Ca2+ sensitivity without increasing the heart rate. [3]
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].
Lidocaine-d10 (Lignocaine-d10) hydrochloride is the deuterium labeled Lidocaine hydrochloride. Lidocaine hydrochloride (Lignocaine hydrochloride) inhibits sodium channels involving complex voltage and using dependence[1]. Lidocaine hydrochloride decreases growth, migration and invasion of gastric carcinoma cells via up-regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. Lidocaine hydrochloride is an amide derivative commonly used to anesthetize. hydrochloride is a a drug to treat ventricular arrhythmia and an effective tumor-inhibitor[2].
(rel)-AR234960 is an active relative configuration of AR234960. AR234960, a non-peptide MAS (a G protein-coupled receptor) agonist, increases both mRNA and protein levels of CTGF via ERK1/2 signaling in HEK293-MAS cells and adult human cardiac fibroblasts[1].
Mibefradil dihydrochloride is a calcium channel blocker with moderate selectivity for T-type Ca2+ channels displaying IC50s of 2.7 μM and 18.6 μM for T-type and L-type currents, respectively.
Gavestinel (GV 150526) is a potent, selective, orally active and non-competitive antagonist of NMDA receptor. Gavestinel binds to the glycine site of the NMDA receptor, with a pKi of 8.5. Gavestinel can be used for the research of acute ischemic stroke[1].
DDO-02001 is a moderately potent Kv1.5 potassium channel inhibitor with an IC50 value of 17.7 μM. DDO-02001 can be used for researching anti-arrhythmia[1].
GPVI antagonist 1 (compound 5) is a glycoprotein VI (GPVI) platelet receptor antagonist. GPVI antagonist 1 inhibits collagen-induced platelet aggregation with an IC50 of 25.3 μM[1].
Ataprost (ONO 41483) is an orally active Carboprostacyclin (HY-112322) analogue. Ataprost exhibits 2.6 times more active than Carboprostacyclin in inhibiting ADP-induced platelet aggregation in vitro. Ataprost has the ability to relieve coronary spasm[1].
Sitaxsentan (sodium) is an orally active, highly selective antagonist of endothelin A receptors.