myocytes

AZD 7009 is a novel antiarrhythmic compound that inhibits the sodium current of hNav1.5 in CHO K1 cells with an IC50 of 11 uM. AZD 7009 inhibited late sodium current in isolated rabbit atrial and ventricular myocytes, and prolonged E-4031-induced action potential duration, promoting early post-depolarization of Purkinye fibers (EADs).

Oxodipine, a dihydropyridine-type calcium antagonist, inhibited KCl-induced aortic contraction in rabbits and reduced cardiac force in less potent rat ventricular test-paper contractions. In rat cultured neonatal ventricular myocytes, Oxodipine reduced L-type Ca currents (I) with an IC of 0.24 μM, and against T-type Ca currents (I) with an IC of 0.41 μM. Oxodipine causes constipation in mice and gingival hyperplasia in dogs.

Amiodarone hydrochloride is an anti-anginal agent and a class III antiarrhythmic drug that inhibits potassium channels (including wild-type hERG channels and their tail currents, with an IC₅₀ of approximately 45 nM) as well as voltage-gated sodium channels. This leads to prolonged action potential duration in ventricular and atrial myocytes, resulting in reduced heart rate and vascular resistance. It activates ERK1 2 and p38 MAPK signaling pathways in fibroblasts, promoting cell proliferation and myofibroblast differentiation. Amiodarone hydrochloride is widely used in the study of supraventricular and ventricular arrhythmias and can also be used to establish pulmonary fibrosis animal models.

Levosimendan (OR1259) is a calcium sensitizer used in the management of acutely decompensated congestive heart failure. It increases the sensitivity of the heart to calcium, thus increasing cardiac contractility without a rise in intracellular calcium. Levosimendan exerts its effect by increasing calcium sensitivity of myocytes by binding to cardiac troponin C in a calcium-dependent manner.

(±)-Naringenin (Naringenine) is a natural product. It displays vasorelaxant effect on endothelium-denuded vessels via the activation of BKCa channels in myocytes.

Reverse T3 (3,3',5'-triiodo-L-thyronine) inhibits the increase of sodium current generated by other thyroid hormone analogs in neonatal rat myocytes.

HMR 1556 is a chromanol derivative and is an IKs blocker (IC50s of 10.5 nM and 34 nM in canine and guinea pig left ventricular myocytes, respectively).

SBI-477 is a chemical probe that stimulates insulin signaling by deactivating the transcription factor MondoA. It coordinately inhibits triacylglyceride (TAG) synthesis and enhances basal glucose uptake in human skeletal myocytes.

Flindokalner (BMS-204352) is a potassium channel modulator and a positive modulator of all neuronal Kv7 channel subtypes expressed in HEK293 cells. It is also a positive modulator of large conductance calcium-activated K channels (BKca) and displays negative modulatory activity at Kv7.1 channels (Ki = 3.7 μM). Additionally, Flindokalner acts as a negative modulator of GABAA receptors and demonstrates anxiolytic efficacy in vivo.

SIRT3 Activator 1 (Compound 5v) is a selective activator of SIRT3. It enhances the expression of SIRT3, leading to upregulation of SOD2 and OPA1. This activity effectively mitigates mitochondrial dysfunction, alleviates oxidative stress, and maintains the vitality of cardiac myocytes. SIRT3 Activator 1 is useful in the study of cardiovascular diseases.

GP-515 HCl is an adenosine kinase inhibitor. In cultured rat myocardial myocytes (RMMs), GP-515 can induce the expression of vascular endothelial growth factor (VEGF). Under severe hypoxia (1% O(2)), GP-515 (20 microM) does not affect VEGF protein expression, but under mild hypoxic conditions, it increases VEGF expression by 27%.

GS967 is a potent, and selective inhibitor of cardiac late sodium current (late INa ).

SIM-6080 is a calcium channel antagonist. SIM-6080 inhibits the proliferation of rat aortic myocytes.

α-Lipoic acid is a cyclic disulfide antioxidant that interconverts with its reduced dithiol form. It is an essential cofactor for decarboxylation reactions of the citric acid cycle and acts as a general antioxidant. AN-7 is a more lipophilic analog of α-lipoic acid with enhanced potency and 1.5-fold increased maximal capacity to stimulate glucose transport into myocytes. This identifies the analogs of lipoic acid as potential new treatments for diabetes.

Sematilide hydrochloride (CK-1752) is a class III antiarrhythmic. It is a selectively delayed rectifier K+ current (IKr) channel blocker. It inhibits rapidly activating Ik in guinea pig atrial myocytes, resulting in the prolongation of refractoriness and action potential duration.

(Sar¹)-Angiotensin II acetate, an analogue of Angiotensin II, is a specific agonist of angiotensin AT1 receptor. It binds to brain membrane-rich particles, with a Kd of 2.7 nM. It can stimulate protein synthesis and cell growth in embryonic chick myocytes.

Tyr-α-CGRP is an N-terminal extended tyrosinated analogue of α-calcitonin gene-related peptide . It binds to amylin receptors AMY1 and AMY3 in COS-7 cells expressing the human receptors (IC50s = 141 and 1.86 nM, respectively). Tyr-α-CGRP also binds to and stimulates cAMP accumulation in rat L6 myocytes (IC50 = 4 nM; EC50 = 12 nM). It also binds to rat brain and spleen membrane preparations (IC50s = 0.2 and 0.5 nM, respectively), induces positive chronotropic and inotropic effects in isolated right and left guinea pig atria (EC50s = 282 and 74 nM, respectively), and inhibits the twitch response in rat vas deferens (EC50 = 1.9 nM).

Ru360, an oxygen-bridged dinuclear ruthenium amine complex, is a selective mitochondrial calcium uptake inhibitor. Ru360 potently inhibits Ca2+ uptake into mitochondria with an IC50 of 0.184 nM. Ru360 binds to mitochondria with high affinity (Kd of 0.34 nM). Ru360 has antiarrhythmic and cardioprotective effects[1][2]. Ru360 permeates slowly into the cell, and specifically inhibits mitochondrial calcium uptake in intact cardiomyocytes and in isolated heart. 1 μm Ru360 is taken up by myocardial cells and accumulated in the cytosol in a biphasic manner[1]. During pelleting hypoxia, Ru360 (10 µM) significantly improves cell viability in wild type cardiomyocytes[3]. Ru360 (15-50 nmol/kg) treatment abolishes the incidence of arrhythmias and haemodynamic dysfunction elicited by reperfusion in a whole rat model. Ru360 administration partially inhibits calcium uptake, preventing mitochondria from depolarization by the opening of the mitochondrial permeability transition pore (mPTP)[1]. [1]. G de J García-Rivas, et al. Ru360, a Specific Mitochondrial Calcium Uptake Inhibitor, Improves Cardiac Post-Ischaemic Functional Recovery in Rats in Vivo. Br J Pharmacol. 2006 Dec;149(7):829-37. [2]. M A Matlib, et al. Oxygen-bridged Dinuclear Ruthenium Amine Complex Specifically Inhibits Ca2+ Uptake Into Mitochondria in Vitro and in Situ in Single Cardiac Myocytes. J Biol Chem. 1998 Apr 24;273(17):10223-31. [3]. Lukas J Motloch, et al. UCP2 Modulates Cardioprotective Effects of Ru360 in Isolated Cardiomyocytes During Ischemia. Pharmaceuticals (Basel). 2015 Aug 4;8(3):474-82.

Arachidonic acid (Immunocytophyt) is a polyunsaturated omega-6 essential fatty acid that serves as a major component of biological membranes and animal phospholipids. It is synthesized from dietary linoleic acid and acts as a precursor to lipid mediators such as prostaglandins, thromboxanes, and leukotrienes. Arachidonic acid can improve cognitive responses and cardiovascular function and is commonly used to induce paw edema models.

SR-33805 is a calcium channel antagonist potentially for the treatment of atherosclerosis and heart failure. SR-33805 restored the MI-altered cell shortening without affecting the Ca(2+) transient amplitude, suggesting an increase of myofilament Ca(2+) sensitivity in MI myocytes. A SR33805-induced sensitization of myofilament activation was found to be associated with a slight increase in myosin light chain-2 phosphorylation and a more significant decrease on troponin I (TnI) phosphorylation. Decreased TnI phosphorylation was related to inhibition of protein kinase A activity by SR-33805.

RFRP-1(human) TFA, an endogenous NPFF receptor agonist, exhibits potent activity with EC50 values of 0.0011 nM for NPFF2 and 29 nM for NPFF1. It significantly diminishes the contractile function of isolated rat and rabbit cardiac myocytes. Moreover, it decreases heart rate, stroke volume, ejection fraction, and cardiac output, while elevating plasma prolactin levels in rats.

Jingzhaotoxin-II, a neurotoxin composed of 32 amino acid residues featuring two acidic and two basic residues, selectively inhibits voltage-gated sodium channels (VGSC), notably slowing the rapid inactivation of TTX-resistant (TTX-R) VGSC in cardiac myocytes, with an IC50 of 0.26 μM [1].

Atrial Natriuretic Peptide (ANP) (1-28), human, porcine Acetate is an atrial natriuretic peptide (ANP) hormone secreted by atrial myocytes that is capable of acting as an natriuretic peptide receptor-A(NPR-A) agonist, used in the treatment of acute decompensated heart failure (ADHF). By binding to specific receptors on the surface of the kidney, blood vessel, and heart cells, Carperitide causes an increase in cyclic guanosine monophosphate (cGMP) levels and induces vasodilatation, diuresis, and sodium excretion, which in turn reduces the heart's workload.

Potent bombesin receptor agonist (IC50 values are 0.26, 1.55 and 2.52 nM for BB1, BB2 and BB3 respectively). Enhances glucose transport in obese and diabetic primary myocytes. Also stimulates NCI-H1299 lung cancer cell proliferation in vitro.