Angina

Bepridil hydrochloride (CERM 1978; Org 5730 hydrochloride) is an orally active non-selective calcium channel antagonist with multi-ion channel blocking activity. Bepridil hydrochloride modulates Calmodulin, the 20S proteasome, T-type/L-type calcium channels, cardiac sodium channels, multiple potassium channels, γ-secretase, β-secretase, and mitoK_ATP/sarcK_ATP channels. Bepridil hydrochloride acts as a hydroxyl radical scavenger, regulates mitochondrial and intracellular calcium handling, and exerts antiarrhythmic, antianginal, and cardioprotective effects. Bepridil hydrochloride alters amyloid precursor protein processing, reduces β-amyloid and thalamic calcium levels, restores seladin-1/DHCR24 expression, and improves sensorimotor recovery after cerebral ischemia. Bepridil hydrochloride also exhibits potent inhibitory effects on SARS-CoV-2 replication. Bepridil hydrochloride is used in studies related to stable angina, arrhythmias, cerebral ischemia, Alzheimer's disease, and SARS-CoV-2 infection.

(S)-(-)-Propranolol hydrochloride is the active isomer of Propranolol (HY-B0573B), with 98-fold greater activity than (R)-(+)-Propranolol. (S)-(-)-Propranolol hydrochloride produces antinociception-related phenotypes in mouse models, accompanied by sedative and ataxic side effects. (S)-(-)-Propranolol hydrochloride can be used in research related to hypertension, myocardial infarction, and pain.

Bepridil (CERM 1978 (free base); Org 5730) is an orally active non-selective calcium channel antagonist with multi-ion channel blocking activity. Bepridil modulates Calmodulin, the 20S proteasome, T-type/L-type calcium channels, cardiac sodium channels, multiple potassium channels, γ-secretase, β-secretase, and mitoK_ATP/sarcK_ATP channels. Bepridil acts as a hydroxyl radical scavenger, regulates mitochondrial and intracellular calcium handling, and exerts antiarrhythmic, antianginal, and cardioprotective effects. Bepridil alters amyloid precursor protein processing, reduces β-amyloid and thalamic calcium levels, restores seladin-1/DHCR24 expression, and improves sensorimotor recovery after cerebral ischemia. Bepridil also exhibits potent inhibitory effects on SARS-CoV-2 replication. Bepridil is used in studies related to stable angina, arrhythmias, cerebral ischemia, Alzheimer's disease, and SARS-CoV-2 infection.

Bepridil hydrochloride hydrate (CERM 1978 hydrate; Org 5730 hydrochloride hydrate) is an orally active non-selective calcium channel antagonist with multi-ion channel blocking activity. Bepridil hydrochloride hydrate modulates Calmodulin, the 20S proteasome, T-type/L-type calcium channels, cardiac sodium channels, multiple potassium channels, γ-secretase, β-secretase, and mitoK_ATP/sarcK_ATP channels. Bepridil hydrochloride hydrate acts as a hydroxyl radical scavenger, regulates mitochondrial and intracellular calcium handling, and exerts antiarrhythmic, antianginal, and cardioprotective effects. Bepridil hydrochloride hydrate alters amyloid precursor protein processing, reduces β-amyloid and thalamic calcium levels, restores seladin-1/DHCR24 expression, and improves sensorimotor recovery after cerebral ischemia. Bepridil hydrochloride hydrate also exhibits potent inhibitory effects on SARS-CoV-2 replication. Bepridil hydrochloride hydrate is used in studies related to stable angina, arrhythmias, cerebral ischemia, Alzheimer's disease, and SARS-CoV-2 infection.

Bevantolol hydrochloride (SOM3355) is a selective β1-adrenergic receptor antagonist, with an IC₅₀ of 35 nM for β₁-adrenergic receptor and an IC₅₀ of 60 nM for VMAT2. Bevantolol hydrochloride blocks β1-adrenergic receptors, exerts partial agonistic effects on α-adrenoceptor, inhibits calcium currents in the sinoatrial and atrioventricular nodes as well as sodium currents in cardiomyocytes, delays repolarization, and shortens the action potential duration of Purkinje cells. Bevantolol hydrochloride reduces peripheral vascular resistance, increases subendocardial blood flow, inhibits VMAT2, elevates the serum HDL/LDL ratio, and does not affect glomerular filtration rate or cause cold extremities. Bevantolol hydrochloride is applicable to research related to angina pectoris, hypertension, arrhythmia, and Huntington's disease.

Bevantolol (SOM3355 (free base)) is a selective β1-adrenergic receptor antagonist, with an IC₅₀ of 35 nM for β₁-adrenergic receptor and an IC₅₀ of 60 nM for VMAT2. Bevantolol blocks β1-adrenergic receptors, exerts partial agonistic effects on α-adrenoceptor, inhibits calcium currents in the sinoatrial and atrioventricular nodes as well as sodium currents in cardiomyocytes, delays repolarization, and shortens the action potential duration of Purkinje cells. Bevantolol reduces peripheral vascular resistance, increases subendocardial blood flow, inhibits VMAT2, elevates the serum HDL/LDL ratio, and does not affect glomerular filtration rate or cause cold extremities. Bevantolol is applicable to research related to angina pectoris, hypertension, arrhythmia, and Huntington's disease.

Etafenone is an antiarrhythmic agent and vasodilator. Etafenone exerts β-adrenergic agonistic effects. Etafenone inhibits the automaticity of sinoatrial nodes, atrioventricular junctions and Purkinje fibers, prolongs action potential duration and refractory period, slows the rising rate of action potentials, and prolongs conduction time. Etafenone enhances collateral circulation after coronary occlusion and suppresses ventricular premature beats. Etafenone delays ischemic myocardial energy imbalance, improves the recovery of high-energy phosphates after ischemia, and reduces myocardial oxygen consumption. Etafenone can be used in research related to ischemic heart disease, arrhythmia and angina pectoris.

Human UGT2B4 is a UDP-glucuronosyltransferase. UGT2B4 catalyzes the glucuronidation of bile acids, Carvedilol (HY-B0006) and 6-hydroxylated bile acids to form glucuronide derivatives. UGT2B4 participates in the inactivation of endogenous and exogenous substances, including catechol estrogens, C19 steroids, phenols and monoterpenoids. Human UGT2B4 can be used in the research of hypertension, angina pectoris, chronic heart failure and intrahepatic cholestasis.

Pranidipine (OPC-13340) is an orally active L-type voltage-dependent calcium channel (L-VDCC) blocker with a K_i value of 0.16 nM. Pranidipine inhibits calcium-induced contraction, suppresses slow-response action potentials, shortens action potential duration, reduces systolic and diastolic blood pressure, and exerts vasodilatory effects. Pranidipine enhances its vasodilatory effect by blocking NO decomposition. Pranidipine can be used in research related to essential hypertension, angina pectoris, myocardial infarction, and dilated cardiomyopathy.

Trapidil (AR-12008) is an orally active vasodilator and antiplatelet agent. Trapidil antagonizes platelet-derived growth factor (PDGF), inhibits phosphodiesterase, thromboxane A₂ synthesis and pro-inflammatory cytokine production. Trapidil promotes prostacyclin biosynthesis, reduces lipid peroxidation, regulates nitric oxide metabolism, and inhibits cell proliferation and migration. Trapidil exerts tissue-protective effects, regulates bone turnover, and inhibits pyroptosis via the GPX3/Nrf2 pathway. Trapidil is applicable to research related to renal ischemia-reperfusion injury, chronic stable angina, restenosis, meningioma, diabetic cardiomyopathy and peripheral nerve crush injury.

Praeruptorin A ((+)-Praeruptorin A) is an orally active isomer of (±)-Praeruptorin A (HY-N0081). Praeruptorin A also acts as a Calcium channel blocker. Praeruptorin A can be isolated from Peucedanum. Praeruptorin A serves as a substrate for CYP3A4. Praeruptorin A downregulates NMDA receptors containing GluN2B and inhibits neuronal Apoptosis. Praeruptorin A mediates vasodilation, inhibits vascular hypertrophy and reduces blood pressure. Praeruptorin A can be used in research related to neurological diseases, myocardial ischemia, heart failure, exertional angina, renovascular hypertension and spontaneous hypertension.

Hydroxytanshinone IIA is a hydrolytic metabolite of Tanshinone IIA (HY-N0135). Tanshinone IIA inhibits angiogenesis by targeting the protein kinase domain of VEGF/VEGFR2. Hydroxytanshinone IIA exhibits antioxidant and anti-inflammatory activities. Hydroxytanshinone IIA can be used in studies of angina pectoris and myocardial infarction.

Cetiedil is a vasodilator and potassium channel blocker with anti-sickle cell and analgesic activities. Cetiedil increases cyclic adenosine monophosphate levels, relaxes vascular smooth muscle, and blocks the action of Bradykinin (HY-P0206). Cetiedil inhibits platelet aggregation, reduces plasma fibrinogen concentration and blood viscosity, suppresses sickling of sickle red blood cells and improves their filterability, and decreases irreversible sickle cells. Cetiedil binds to calmodulin, inhibits Ca²⁺-dependent potassium permeability of erythrocyte membranes, increases sodium permeability of erythrocytes, and regulates polymorphonuclear leukocyte function. Cetiedil can be used in research related to intermittent claudication, arteriosclerosis obliterans, diabetic arteriosclerosis, Raynaud's disease, angina pectoris, and sickle cell anemia.

Bromelain USP is an orally active proteolytic agent. Bromelain USP converts plasminogen to plasmin to support fibrinolysis, cleaves CD44 adhesion molecules from cell surfaces, and diminishes uPAR expression and uPA activity. Bromelain USP can inhibit the activity of a variety of fungi and bacteria. Bromelain USP can be used for the research of angina pectoris, atherosclerotic disease, fungal infections, bacterial infections, chronic inflammatory bowel disease, and cancer.

Chromonar hydrochloride (Carbocromen hydrochloride) is an orally active, selective long-acting coronary vasodilator. Chromonar hydrochloride increases coronary blood flow. Chromonar hydrochloride is used for the research of angina pectoris.

(R)-Niguldipine, a R-epimer of Niguldipine (HY-101390B), is a calcium channel antagonist. (R)-Niguldipine exerts a vasodilatory effect by blocking calcium channels and reducing the transmembrane influx of calcium ions. (R)-Niguldipine can inhibit U-46619 (HY-108566)-induced coronary artery contraction in guinea pig Langendorff hearts (pID₅₀ of 9.93), has high affinity for calcium channel binding sites on guinea pig skeletal muscle membranes (K_i of 8.10), and lowers blood pressure in spontaneously hypertensive rats (pED₃₀ of 5.55). (R)-Niguldipine can improve cardiovascular diseases such as hypertension, angina pectoris, and arrhythmias.

Ivabradine sulfate is a potent and orally active HCN (hyperpolarization-activated cyclic nucleotide-gated) channel blocker that inhibits the cardiac pacemaker current (If). Ivabradine sulfate reduces dose-dependently heart rate without modification of blood pressure. Ivabradine sulfate shows anticonvulsant, anti-ischaemic and anti-anginal activity.

Propatyl nitrate is a coronary vasodilator. Propatyl nitrate is also a nitric oxide donor. Propatyl nitrate can be used in research on cardiovascular and cerebrovascular diseases such as acute angina attacks.

N-PTyrosine PA (N-Palmitoyl-tyrosine phosphoric acid) ammonium is a lysophosphatidic acid (LPA) receptor modulator, which exhibits weak inhibitory activity against LPA1 and partial agonist properties towards LPA5. N-PTyrosine PA ammonium inhibits the activation of LPA receptors and downstream responses by competing with agonists for binding sites. N-PTyrosine PA ammonium can induce morphological changes and aggregation, and also inhibit LPA-induced morphological changes through receptor desensitization caused by pre-incubation. N-PTyrosine PA ammonium can be used in the research of related diseases such as atherosclerosis and acute ischemic syndromes (e.g., unstable angina, myocardial infarction, stroke).

(-)-Niguldipine ((R)-Niguldipine) hydrochloride is a calcium channel antagonist. (-)-Niguldipine hydrochloride exerts a vasodilatory effect by blocking calcium channels and reducing the transmembrane influx of calcium ions. (-)-Niguldipine can inhibit U-46619 (HY-108566)-induced coronary artery contraction in guinea pig Langendorff hearts (pID₅₀ of 9.93), has high affinity for calcium channel binding sites on guinea pig skeletal muscle membranes (K_i of 8.10), and lowers blood pressure in spontaneously hypertensive rats (pED₃₀ of 5.55). (-)-Niguldipine hydrochloride can improve cardiovascular diseases such as hypertension, angina pectoris, and arrhythmias.