isoproterenol

Isoproterenol (Norisodrine) is a non-selective and orally active β-adrenoceptor agonist.Isoproterenol is a potent peripheral vasodilator and bronchodilator.Isoproterenol can be used in the study of bradycardia and bronchial asthma for the treatment of heart block, bradycardia.

Isoproterenol sulfate anhydrous is a useful alkaloid. It is used for biological research.

(S)-Isoproterenol bitartrate is a bioactive chemical.

Isoproterenol tartrate, (-)- is a beta-Adrenoceptor agonist agent that increases cytosolic cAMP.

Isoproterenol-d7 is intended for use as an internal standard for the quantification of isoproterenol by GC- or LC-MS. Isoproterenol is an agonist of β1- and β2-adrenergic receptors (β1- and β2-ARs; Kis = 224 and 458 nM, respectively). It is selective for β1- and β2-ARs over β3-ARs (Ki = 1,570 nM). Isoproterenol inhibits contractions in isolated field-stimulated rat vas deferens (EC50 = 45.6 nM). In vivo, isoproterenol (0.33 mg/kg) decreases blood pressure and increases water intake in nephrectomized rats. It reduces blood pressure and increases heart rate in renal hypertensive rabbits. Isoproterenol inhibits histamine-induced bronchospasms in anesthetized dogs. Formulations containing isoproterenol have been used in the treatment of bradydysrhythmias and to improve breathing during anesthesia.

(-)-Isoproterenol hydrochloride is used as a β-adrenergic receptor agonist in the treatment of bradycardia and as a bronchodilator.

Isoproterenol bitartrate is a beta-sympathomimetic and an isopropyl analog of Epinephrine, which acts on the heart, bronchi, skeletal muscle, and alimentary tract. It is used mainly as a bronchodilator and heart stimulant.

Isoprenaline hydrochloride (NCI-c55630) is a potent beta-adrenergic agonist with the peripheral vasodilator, bronchodilator, and cardiac stimulating properties.

Bisaramil hydrochloride (Bisaramil) is a novel diazabicyclononane antiarrhythmic compound that inhibits the generation of free radicals.Bisaramil hydrochloride blocks sodium currents and inhibits the slow Ca(2+) action potential induced by isoproterenol in K(+)-depolarized muscle.

Dichloroisoproterenol is also known as Dichloroisoprenaline (DCI), was the first beta blocker ever to be developed. It is non-selective for the β1-adrenergic and β2-adrenergic receptors. DCI has low potency and acts as a partial agonist/antagonist at these receptors. Dichloroisoprenaline is a racemic mixture of enantiomers.

Dichloroisoproterenol hydrochloride is a biochemical. It may be used for cardiac arrhythmia.

Sinapinic Acid (Synapoic acid) protects the rat liver from CCl4-induced inflammation, most likely by acting as a free radical scavenger and modulator of NF-κB p65 activation and proinflammatory cytokine expression. Sinapic acid with antioxidant role protects cardiac cells and its functions from I/R induced oxidative stress. Sinapic acid is a potentially useful agent for the protection against liver fibrosis and cirrhosis. Sinapic acid prevents the alterations in the levels of lipids and lipoproteins by virtue of its anti-lipidaemic effect in isoproterenol induced myocardial infarcted rats. Sinapic acid ameliorates hyperglycemia through PLC-PKC signals to enhance the glucose utilization in diabetic rats.

FFA2 allosteric agonist. Inhibits forskolin-induced cAMP increase and stimulates 35SGTPγS binding in biochemical assays (pEC50 values are 6.9 and 7.23, respectively). Binds at allosteric binding site. In functional assays, displays positive allosteric modulation of FFA-induced Gi signaling and negative allosteric modulation of FFA-induced Gq/G11 signaling. Inhibits lipolytic effect of isoproterenol (pEC50 = 5.03) and induces migration of human neutrophils in vitro. Bolognini et al (2016) A novel allosteric activator of free fatty acid 2 receptor displays unique Gi-functional bias. J.Biol.Chem. 291 18915 PMID:27385588 |Sergeev et al (2017) A single extracellular amino acid in free fatty acid receptor 2 defines antagonist species selectivity and G protein selection bias. Sci.Rep. 7 13741 PMID:29061999

Fenspiride-d5 is intended for use as an internal standard for the quantification of fenspiride by GC- or LC-MS. Fenspiride is an antagonist of histamine H1 receptors and a non-steroidal anti-inflammatory drug (NSAID). It inhibits histamine-induced contraction of isolated guinea pig trachea but not histamine-induced inotropy of isolated guinea pig heart. It also inhibits phosphodiesterase 4 (PDE4), PDE5, and PDE3 (IC50s = 69, ~158, and 363 µM, respectively, in isolated human bronchi derived from patients with lung cancer). It is selective for these phosphodiesterases over PDE1 and PDE2, where it provides less than 25% inhibition. Fenspiride potentiates the airway relaxant effects of isoproterenol and sodium nitroprusside indicating an effect on cAMP and cGMP phosphodiesterases, respectively. Aerosolized fenspiride (1 mg/ml) reverses bronchoconstriction induced by capsaicin and, when used at aerosolized concentrations ranging from 1-10 mg/ml, reduces cough induced by citric aci......

Clofeverine hydrochloride is the salt form of Clofeverine (free base), a highly selective relaxant for gastrointestinal smooth muscles with a beta-receptor stimulative nature. On isolated ileum, the inhibitory effect of clofeverine for spontaneous motility was comparable to that of isoproterenol and 100 times higher than that of papaverine.

SB 204741 is a selective 5-HT2B antagonist with high affinity and pKi value of 7.1.

Protokylol hydrochloride is the salt form of Protokylol (free base) (Asmetil, Caytine, Palison, Ventaire), a β-adrenergic receptor agonist used as a bronchodilator in Europe and the United States. It is methylenedioxyphenyl-isoproterenol.

Clofeverine (free base) is a highly selective relaxant for gastrointestinal smooth muscles with a beta-receptor stimulative nature. On isolated ileum, the inhibitory effect of clofeverine for spontaneous motility was comparable to that of isoproterenol and 100 times higher than that of papaverine.

Rp-cAMPS sodium salt, a cAMP analog, is a potent, competitive cAMP-induced activation of cAMP-dependent PKA I and II (Kis of 12.5 μM and 4.5 μM, respectively) antagonist. Rp-cAMPS sodium salt is resistant to hydrolysis by phosphodiesterases[1][2][3][4][5][6]. A membrane-permeable competitive cAMP antagonist (Rp-cAMPS) that blocks PKA activation by binding to the regulatory subunits without dissociating the kinase holoenzyme also inhibits synaptic plasticity but has no effect on normal synaptic transmission[2]. Rp-cAMPS (10 μM, 15 min) decreases the monosynaptic EPSCs evoked at the PB-CeLC and BLA-CeLC synapses in slices from arthritic rats but not in control neurons from normal animals. The inhibitory effect of Rp-cAMPS is significant compared to predrug (ACSF) control values obtained in the same neurons[2]. [1]. R J de Wit, et al. Inhibitory action of certain cyclophosphate derivatives of cAMP on cAMP-dependent protein kinases. Eur J Biochem. 1984 Jul 16;142(2):255-60. [2]. Rothermel JD, et al. A mechanistic and kinetic analysis of the interactions of the diastereoisomers of adenosine 3’,5’-(cyclic)phosphorothioate with purified cyclic AMP-dependent protein kinase. Biochem J. 1988 May 1;251(3):757-62.[3]. Fu Y, et al. PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior. Mol Pain. 2008 Jul 16;4:26.[4]. Kuriyama S, et al. Isoproterenol inhibits rod outer segment phagocytosis by both cAMP-dependent and independent pathways. Invest Ophthalmol Vis Sci. 1995 Mar;36(3):730-6.[5]. Dostmann WR, et al. Probing the cyclic nucleotide binding sites of cAMP-dependent protein kinases I and II with analogs of adenosine 3’,5’-cyclic phosphorothioates. J Biol Chem. 1990 Jun 25;265(18):10484-91.[6]. Van Haastert PJ, et al. Competitive cAMP antagonists for cAMP-receptor proteins. J Biol Chem. 1984 Aug 25;259(16):10020-4.

Rimiterol, a beta 2 stimulant, therefore affects the cardiovascular system less than isoproterenol.

Cyclic ADP-ribose (cADP-ribose) is an endogenous metabolite of NAD+ that mobilizes the release of stored Ca2+ in the endoplasmic reticulum via ryanodine receptors in various cell types.[1],[2],[3],[4],[5] This second messenger is generated via the cADP-ribose synthases CD38 and CD157.[6],[5],[7] cADP-Ribose may also trigger the cell surface Ca2+ influx channel TRPM2 in a temperature-dependent manner.[8] In vitro, cADP-ribose modulates Ca2+ signaling in rat and mouse cardiomyocytes treated with isoproterenol , and treatment with this metabolite at 100 μM under heat stress conditions induces the release of oxytocin from the mouse hypothalamus.[9],[4]