product name Netarsudil (AR-13324)
Description: Netarsudil (also known as a.k.a. AR-13324) is ROCK inhibitor with Ki value of 0.2-10.3 nM. It is currently in clinical trials for the treatment of glaucoma and ocular hypertension. Previous study showed that at the cellular level, netarsudil had been shown to be able to induce loss of actin stress fibers, cell shape changes, loss of focal adhesions, as well as changes in extracellular matrix composition of TM cells. Netarsudil primarily targets cells in the conventional outflow tract, efficiently decreasing IOP in both human and non-human primate eyes. In addition, netarsudil has been shown to increase outflow facility in non-human primate eyes and to decrease episcleral venous pressure in rabbit eyes.
References: Eur J Pharmacol. 2016 Sep 15;787:20-31; Invest Ophthalmol Vis Sci. 2016 Nov 1;57(14):6197-6209.
526.45
Formula
C28H27N3O3.2HCl
CAS No.
1253952-02-1
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 20 mg/mL (38 mM)
Water: 54 mg/mL (102.6 mM)
Ethanol: 2 mg/mL (3.8 mM)
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: Previous study showed that at the cellular level, netarsudil had been shown to be able to induce loss of actin stress fibers, cell shape changes, loss of focal adhesions, as well as changes in extracellular matrix composition of TM cells Kinase Assay: Cell Assay: Previous study showed that at the cellular level, netarsudil had been shown to be able to induce loss of actin stress fibers, cell shape changes, loss of focal adhesions, as well as changes in extracellular matrix composition of TM cells. |
|---|---|
| In Vivo | Animal efficacy study found that the topical treatment of netarsudil was able to affect both proximal (trabecular meshwork and Schlemms Canal) and distal portions (intrascleral vessels) of the mouse conventional outflow tract. |
| Animal model | |
| Formulation & Dosage | |
| References | Eur J Pharmacol. 2016 Sep 15;787:20-31; Invest Ophthalmol Vis Sci. 2016 Nov 1;57(14):6197-6209. |
