outflow

BAY 73-1449 is a potent and selective antagonist of the prostacyclin receptor (IC50 < 0.1 nM).

Neuropeptide W-30 (human) serves as a crucial stress mediator within the central nervous system, influencing the hypothalamus-pituitary-adrenal (HPA) axis and sympathetic outflow. It acts as an endogenous ligand for the two related orphan G-protein-coupled receptors (GPCRs), GPR7 and GPR8, binding and activating them at comparable effective doses [1] [2] [3].

δ14-Triamcinolone acetonide is a potential impurity found in commercial preparations of triamcinolone acetonide. Triamcinolone acetonide is a synthetic corticosteroid. It decreases cytokine levels, the firing rate of sensory neurons, and mechanical hypersensitivity in a rat spinal nerve ligation model when used at a dose of 1.5 mg/kg prior to and following surgery for three days. Triamcinolone acetonide also decreases outflow facility in a mouse model of steroid-induced glaucoma when 20 μl of a 40 mg/ml suspension is administered subconjunctivally. Formulations containing triamcinolone acetonide are used in the treatment of diabetic macular edema.

P-gb-IN-1 is a potent P-glycoprotein (P-gp) inhibitor that exhibits reverse activity by inhibiting P-gp outflow. P-gb-IN-1 has been shown to inhibit P-gp by hydrogen bonding with residues Asn 721 and Met 986. P-gb-IN-1 showed low toxicity in MCF-7 ADR cells.

Verosudil (AR-12286) is a highly potent Rho kinase (ROCK) inhibitor with a Ki of 2 nM and 2 nM against ROCK1 and ROCK2, respectively. AR-12286 mitigates steroid-induced intraocular pressure in mice by decreasing intraocular pressure through enhanced outflow of aqueous humor via the trabecular meshwork.

Netarsudil, also known as AR-11324, is a Rho-associated protein kinase inhibitor. Netarsudil is potential useful for treating glaucoma and or reducing intraocular pressure. Netarsudil Increases Outflow Facility in Human Eyes Through Multiple Mechanisms. Netarsudil inhibited kinases ROCK1 and ROCK2 with a Ki of 1 nM each, disrupted actin stress fibers and focal adhesions in TM cells with IC50s of 79 and 16 nM, respectively, and blocked the profibrotic effects of TGF-β2 in HTM cells. Netarsudil produced large reductions in IOP in rabbits and monkeys that were sustained for at least 24 h after once daily dosing, with transient, mild hyperemia observed as the only adverse effect.

Nicorandil-d4 is intended for use as an internal standard for the quantification of nicorandil by GC- or LC-MS. Nicorandil is an activator of sulfonylurea receptor 2B (SUR2B) linked to ATP-sensitive potassium channel Kir6.2 (EC50 = ~10 µM) and a nitric oxide (NO) donor. It is selective for SUR2B Kir6.2 over the SUR2A Kir6.2 channel (EC50 = >500 µM). Nicorandil activates soluble guanylate cyclase in a cell-free assay and relaxes partially depolarized isolated bovine coronary artery strips (EC50 = 4.4 µM). It decreases mean blood pressure, coronary resistance, and heart rate, as well as increases coronary sinus outflow, in dogs when administered intravenously at a dose of 1 mg kg. Nicorandil increases survival and decreases infarct size in a rabbit model of myocardial ischemia-reperfusion injury induced by left coronary artery occlusion. Formulations containing nicorandil have been used in the treatment of angina pectoris.

Neuropeptide W-30 (rat) acts as a crucial stress mediator within the central nervous system, influencing the hypothalamus-pituitary-adrenal (HPA) axis and sympathetic outflow. It serves as an endogenous ligand for the two related orphan G-protein-coupled receptors (GPCRs), GPR7 and GPR8. NPW-30 binds and activates both GPR7 and GPR8 at comparable effective doses [1] [2] [3].

(E)-Guanabenz ((E)-Wy-8678), an oral central α2-adrenoceptor agonist, exhibits antihypertensive and neuroprotective activities by stimulating central α2-adrenoceptors to reduce sympathetic outflow and directly inhibiting GADD34. It is used in researching hypertension and Parkinson's disease [1] [2].

Trazium esilate is an adrenergic receptor antagonist. Trazium esilate is a weak displacer on a1-, a2- and D2-receptors, however, it induced a2-receptor desenzitization after repeated treatment. It had no influence on rat brain cortical noradrenaline and s