Transcainide (R 54718) is an orally active antiarrhythmic agent[1].
L-Palmitoylcarnitine chloride, a long-chain acylcarnitine and a fatty acid metabolite, accumulates in the sarcolemma and deranges the membrane lipid environment during ischaemia. L-Palmitoylcarnitine chloride inhibits KATP channel activity, without affecting the single channel conductance, through interaction with Kir6.2[1].
Angiotensin-converting enzyme (ACE) is a dicarboxypeptidase, it converts inactive Angiotensin I (Ang I) to active Ang II and degrades active bradykinin (BK). Angiotensin-converting enzyme is a potent vasoconstrictor, is often used in biochemical studies[1].
Moexipril-d5 is the deuterium labeled Moexipril. Moexipril hydrochloride is a potent orally active non-sulfhydryl angiotensin converting enzyme(ACE) inhibitor, which is used for the treatment of hypertension and congestive heart failure[1][2].
Rev 5975 is a non-sulfhydryl ACE-inhibitor.
Nyasicoside is a norlignan glucosides that can be isolated from Curculigo capitulate. Nyasicoside has potent activity against ouabain-induced arrhythmia in the heart preparations of guinea pig[1].
Siguazodan (SKF 94836) is a potent, selective and orally active phosphodiesterase III (PDE-III) inhibitor with an IC50 of 117 nM. Siguazodan increases cAMP accumulation in intact platelets with an EC50 of 18.88 μM. Siguazodan also inhibits phenylephrine-induced 5-HT release with an IC50 value of 4.2 μM[1][2][3].
Etilefrine hydrochloride is an orally active α adrenergic agonist. Etilefrine hydrochloride is also an AMPK activator. Etilefrine hydrochloride can be used for the research of postural hypotension[1][2][3][4].
Fmoc-His(3-Me)OH derives Histidine-associating compounds with biological activity. Fmoc-His(3-Me)OH, with Fmoc-citrulline-OH, Fmoc-His(1-Me)-OH together, forms tri-peptides and shows vasodilating effect with EC50s of 2.7-4.7 mM in 1.0 mM Phenylephrine (PE)-contracted aorta rings. Fmoc-His(3-Me)OH (resin) also makes Methyl-His-Gly-Lys (His(3-Me)-Gly-Lys), thus acts as an [Ca2+]i inhibitor. Fmoc-His(3-Me)OH methylates NAHIS02, making it unable to block the Alzheimer's Aβ channel[1][2][3].
URAT1 inhibitor 5 (compound 16) is a potent URAT1 inhibitor. URAT1 inhibitor 5 can be used in research of hyperuricemia[1].
BA 41899 is a purely calcium-sensitizing agent. BA 41899 is completely devoid of phosphodiesterase (PDE) III inhibitory activity or any other known inotropic mechanism. BA 41899 can be used for the research of cardiovascular diseases, such as congestive heart failure (CHF)[1].
Sirtuin modulator 4 (compound 12) is a sirtuin modulator. Sirtuin modulator 4 shows inhibitory effect to SIRT1 with an EC50 value of 51-100 μM. Sirtuin modulator 4 may be used for the research of increasing the lifespan of a cell, and preventing a wide variety of diseases and disorders including, for example, diabetes, obesity, neurodegenerative diseases, cardiovascular diseases, inflammation and cancer[1].
Olmesartan medoxomil-d6 (CS 866-d6) is the deuterium labeled Olmesartan medoxomil. Olmesartan medoxomil is a potent and selective angiotensin AT1 receptor inhibitor with IC50 of 66.2 μM[1][2].
Norethindrone acetate is a female progestin approved by FDA for the treatment of endometriosis, uterine bleeding caused by abnormal hormone levels, and secondary amenorrhea.
Clobutinol is a compound that has anti-tussive effects. Clobutinol affects heart rate and blood pressure, it can be used for cough related research[1][2][3].
Efonidipine(NZ-105) Hcl monoethanolate 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].
CHPG is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells[1]. CHPG protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways[2].
HMR 1556, a chromanol derivative, is a IKs blocker with IC50s of 10.5 nM and 34 nM in canine and guinea pig left ventricular myocytes, respectively[1][2].
Evinacumab (REGN1500) is a humanised anti-ANGPTL3 (angiopoietin-like protein 3) monoclonal antibody (IgG4 class antibody). Evinacumab reduces plasma lipids in dyslipidemic mice by blocking ANGPTL3. Evinacumab can be used in studies of homozygous familial hypercholesterolaemia (HoFH), refractory hypercholesterolaemia (both familial and non-familial) and severe hypertriglyceridaemia[1].
Trimetazidine dihydrochloride is a drug for angina pectoris. Trimetazidine is the first cytoprotective anti-ischemic agent , which improves myocardial glucose utilization through inhibition of fatty acid metabolism.
TIE-2/VEGFR-2 kinase-IN-5 is an anti-angiogenic agent. TIE-2/VEGFR-2 kinase-IN-5 also is a potent TIE-2 and VEGFR-2 tyrosine kinase inhibitor with pIC50 values of 7.78 nM and 8.11 nM, respectively. TIE-2/VEGFR-2 kinase-IN-5 can be used for the research of angiogenesis[1].
Nelutroctiv is a potent cardiac troponin activator[1].
Enlicitide chloride is a potent PCSK9 antagonist. Enlicitide chloride can be used for research of cardiovascular disease, e.g. atherosclerosis, hypercholesterolemia, coronary heart disease, metabolic syndrome, acute coronary syndrome, or related cardiovascular disease and cardiometabolic conditions[1][2].
Toringin, a bioflavonoid, is isolated from the bark of Docyniopsis tschonoski. Toringin progressively decreases not only the cis-effect of the expanded CTG repeats but cytotoxicity as well. Exposure to isosakuranetin, Toringin rescues PC12 neuronal cells. Flavonoids are efficacious for ameliorating the RNA gain of function caused by expanded CTG repeats, and have various biological activities and beneficial actions against cancers, coronary heart disease, among other pathologies[1].
GRK2 Inhibitor 1 (methyl 5-[2-(5-nitro-2-furyl)vinyl]-2-furoate) is a GRK2 (β-ARK1) inhibitor[1].
Abicipar pegol (AGN-150998, MP0112) is an anti-VEGF DARPin molecule, a novel class of small proteins containing ankyrin repeat domains engineered to bind with high specificity and affinity to target proteins. Abicipar pegol effectively inhibits angiogenesis and vascular permeability and is used in the study of diseases related to ocular inflammation by intravitreal injection, reducing mean retinal thickness and leakage area[1][2].
FTX-6058 hydrochloride is a potent and orally active inhibitor of Embryonic Ectoderm Development (EED). FTX-6058 hydrochloride can induce HbF protein expression in cell and murine models. FTX-6058 hydrochloride can be used for the research of select hemoglobinopathies, including sickle cell disease and β-thalassemia[1][2].
Efonidipine(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].
BIX 02565 is a potent ribosomal S6 kinase 2 (RSK2) inhibitor with IC50 of 1.1 nM.
Gap 27, connexin43 mimetic peptide, is a gap junction inhibitor.