Ruboxistaurin - CAS 169939-94-0
Catalog number: 169939-94-0
Category: Inhibitor
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Molecular Formula:
C28H28N4O3
Molecular Weight:
468.557
COA:
Inquire
Targets:
PKC
Description:
Ruboxistaurin, also called as LY 333531, initially developed for the treatment of diabetic retinopathy, inhibits isolated enzymes PKCβI and PKCβII with a half-maximal inhibitory constant of 4.5 and 5.9 n M , respectively. The half-life of ruboxistaurin, which can be orally administered, is approximately 9 h and that of its metabolite 16 h, therefore allowing once-daily dosing. Based on data from clinicalTrials.gov, Children's Hospital Medical Center, Cincinnati plan a phase I/II trial of the effect of ruboxistaurin for its safety, tolerability, and effectiveness in treating adult patients with heart failure on June 9, 2016.
Brife Description:
Protein kinase C beta inhibitor
Appearance:
Solid powder
Synonyms:
13-((dimethylamino)methyl)-10,11,14,15-tetrahydro-4,9:16,21-dimetheno-1H,13H-dibenzo(e,k)pyrrolo(3,4-h)(1,4,13)oxadiazacyclohexadecene-1,3(2H)-dione; Arxxant; LY 333531; LY-333531; LY333531; ruboxistaurin; ruboxistaurin mesilate hydrate
Solubility:
Soluble in DMSO
Storage:
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -42℃ for long term (months to years).
MSDS:
Inquire
Shelf Life:
2 years
Boiling Point:
744.4ºC at 760mmHg
Density:
1.34 g/cm3
InChIKey:
ZCBUQCWBWNUWSU-SFHVURJKSA-N
InChI:
1S/C28H28N4O3/c1-30(2)15-18-11-12-31-16-21(19-7-3-5-9-23(19)31)25-26(28(34)29-27(25)33)22-17-32(13-14-35-18)24-10-6-4-8-20(22)24/h3-10,16-18H,11-15H2,1-2H3,(H,29,33,34)/t18-/m0/s1
Canonical SMILES:
CN(C)CC1CCN2C=C(C3=CC=CC=C32)C4=C(C5=CN(CCO1)C6=CC=CC=C65)C(=O)NC4=O
Current Developer:
Eli Lilly; Takeda; Children's Hospital Medical Center and The Christ Hospital
1.Evidence underlying the clinical management of diabetic macular oedema.
Williams MA;Chakravarthy U Clin Med (Lond). 2013 Aug;13(4):353-7. doi: 10.7861/clinmedicine.13-4-353.
Diabetic retinopathy (DR) is the leading cause of visual loss in the developed world in those of working age, and its prevalence is predicted to double by 2025. The management of diabetic retinopathy has traditionally relied on screening, on laser treatment delivered by ophthalmologists, and on optimising blood glucose and blood pressure. Recent evidence suggests that the role of systemic factors is more complex than originally thought, and that drugs such as ACE inhibitors, fibrates and glitazones may all influence the course of diabetic macular oedema. Antagonism of vascular endothelial growth factor offers a new therapeutic avenue that may transform the management of diabetic macular oedema. Several other therapeutic options are under investigation and development, including aminoguanidine, sorbinol, ruboxistaurin and autologous stem cell transfusion.
2.Effects of dexmedetomidine on the release of glial cell line-derived neurotrophic factor from rat astrocyte cells.
Yan M;Dai H;Ding T;Dai A;Zhang F;Yu L;Chen G;Chen Z Neurochem Int. 2011 Apr;58(5):549-57. doi: 10.1016/j.neuint.2011.01.013. Epub 2011 Jan 15.
Dexmedetomidine (DEX) has been found to improve neuronal survival after transient global or focal cerebral ischemia in rats. Astrocyte cells may possess beneficial properties that promote neuronal recovery by secreting neurotrophic factors, such as glial cell line-derived neurotrophic factor (GDNF). The purpose of this study was to investigate the effects of DEX on GDNF release from astrocytes and the possible mechanisms involved. Astrocyte cells were treated with DEX, and GDNF level in the conditioned media was determined by ELISA assay. The expression of CREB, p-CREB and PKCα was analyzed by Western blotting to explore the mechanisms involved in GDNF release. Our results showed that DEX stimulated GDNF release in a time- and dose-dependent manner; and this stimulation was blocked by the α2-adrenoreceptor antagonist yohimbine, but not by α1-adrenoreceptor antagonist prasozin, demonstrating that DEX induced GDNF release likely acts via activating the α2A adrenoreceptor. In addition, DEX-stimulated GDNF release was also blocked by the universal PKC inhibitor Ro-318220 and PKCα/β inhibitor Gö 6976, but not by PKCδ inhibitor rottlerin and PKCβ inhibitor LY333531. Interestingly, DEX also activated CREB phosphorylation, which was inhibited by Ro-318220, Gö 697 and ERK kinase inhibitor PD98059.
3.Inhibition of intraocular neovascularization caused by retinal ischemia in pigs by PKCbeta inhibition with LY333531.
Danis RP;Bingaman DP;Jirousek M;Yang Y Invest Ophthalmol Vis Sci. 1998 Jan;39(1):171-9.
OBJECTIVE: ;The authors tested the antiangiogenic properties of an orally administered protein kinase-Cbeta inhibitor, LY333531, in a pig model of preretinal neovascularization caused by retinal branch vein occlusion to determine the effectiveness of this therapy in preventing intraocular neovascularization from an ischemic stimulus.;METHODS: ;In 20 eyes of 10 pigs, branch retinal vein occlusions were created in a standardized manner using photodynamic thrombosis with rose bengal dye and thermal burns from an argon laser with green light. Five animals received 1 mg/kg LY333531 daily in two oral doses, and five animals were untreated. The eyes were followed clinically for 12 weeks with ophthalmoscopy, fundus photography, and fluorescein angiography. A standardized grading system permitted masked assessment of disc proliferations using stereo fundus photographs. After the pigs were killed, all neovascularization was confirmed histopathologically in a masked fashion and a final grade was assigned to each eye. The Mann-Whitney test was used for statistical analysis of the median values of the unpaired data between the two eyes of each animal (data were rounded up).;RESULTS: ;Significant inhibition of neovascularization was observed in eyes from animals treated with the study drug (P = 0.
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Chemical Structure

CAS 169939-94-0 Ruboxistaurin

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