Nepafenac(AHR9434 AL6515 Nevanac)

Molecular Weight (MW)	254.28
Formula	C15H14N2O2
CAS No.	78281-72-8
Storage	-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)	DMSO: 50 mg/mL (196.6 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Other info	Chemical Name: 2-(2-amino-3-benzoylphenyl)acetamide InChi Key: QEFAQIPZVLVERP-UHFFFAOYSA-N InChi Code: InChI=1S/C15H14N2O2/c16-13(18)9-11-7-4-8-12(14(11)17)15(19)10-5-2-1-3-6-10/h1-8H,9,17H2,(H2,16,18) SMILES Code: O=C(N)CC1=CC=CC(C(C2=CC=CC=C2)=O)=C1N
Synonyms	AHR 9434, AHR 9434; AHR9434; AL 6515; AL-6515; AHR-9434; Nevanac; Nepafenac; Nevanac

Molecular Weight (MW)

254.28

Formula

C15H14N2O2

CAS No.

78281-72-8

Storage

-20℃ for 3 years in powder form

-80℃ for 2 years in solvent

Solubility (In vitro)

DMSO: 50 mg/mL (196.6 mM)

Water: <1 mg/mL

Ethanol: <1 mg/mL

Other info

Chemical Name: 2-(2-amino-3-benzoylphenyl)acetamide

InChi Key: QEFAQIPZVLVERP-UHFFFAOYSA-N

InChi Code: InChI=1S/C15H14N2O2/c16-13(18)9-11-7-4-8-12(14(11)17)15(19)10-5-2-1-3-6-10/h1-8H,9,17H2,(H2,16,18)

SMILES Code: O=C(N)CC1=CC=CC(C(C2=CC=CC=C2)=O)=C1N

Synonyms

AHR 9434, AHR 9434; AHR9434; AL 6515; AL-6515; AHR-9434; Nevanac; Nepafenac; Nevanac

In Vitro	In vitro activity: Nepafenac is a non-steroidal anti-inflammatory drug (NSAID). The IC50 values of nepafenac for (cyclooxygenase-1) COX-1 and COX-2 are 250 nM and 150 nM, respectively. Cell Assay: Nepafenac significantly reduced proliferation rate of human uveal melanoma cell lines including SP6.5, 92.1, OCM-1, MKT-BR and of human transformed uveal melanocyte cell line UW-1. Compared to rofecoxib, nepafenac might reveal a better systemic safety profile.
In Vivo	Nepafenac shows significantly greater ocular bioavailability and amfenac demonstrated greater potency at COX-2 inhibition than ketorolac or bromfenac. Nepafenac exhibits only weak COX-1 inhibitory activity with IC50 of 64.3 mM. Nepafenac inhibits prostaglandin synthesis in the iris/ciliary body (85-95%) and the retina/choroid (55%) in rabbits. Nepafenac (0.5%) produces 65% reduction in retinal edema which is correlated with 62% inhibition of blood-retinal barrier breakdown. Nepafenac (0.5%) significantly inhibits (46%) blood-retinal barrier breakdown concomitant with near total suppression of PGE2 synthesis (96%). Nepafenac significantly inhibits retinal prostaglandin E(2), superoxide, cyclooxygenase-2, and leukostasis within retinal microvessels in insulin-deficient diabetic rats, without affecting vascular endothelial growth factor (VEGF) and nitric oxide (NO). Nepafenac significantly inhibits the number of transferase-mediated dUTP nick-end labeling-positive capillary cells, acellular capillaries, and pericyte ghosts in diabetic rats. Nepafenac results in significantly less choroidal neovascularization and significant less ischemia-induced retinal neovascularization in mice compare to control. Nepafenac also blunts the increase in VEGF mRNA in the retina induced by ischemia. Nepafenac delays the progression of malignancy as well as reduces weight in an ocular and metastatic animal model of uveal melanoma.
Animal model	Nepafenac showed to significantly decrease the retinal levels of PGE2 in LPS-induced rats when administrated topically. However, nepafenac has revealed no significant effect on BRB permeability in LPS-induced rat model
Formulation & Dosage	N/A
References	Inflammation. 2000 Aug;24(4):357-70; Inflammation. 2003 Oct;27(5):281-91; Invest Ophthalmol Vis Sci. 2003 Jan;44(1):409-15.

In Vitro

In vitro activity: Nepafenac is a non-steroidal anti-inflammatory drug (NSAID). The IC50 values of nepafenac for (cyclooxygenase-1) COX-1 and COX-2 are 250 nM and 150 nM, respectively.

Cell Assay: Nepafenac significantly reduced proliferation rate of human uveal melanoma cell lines including SP6.5, 92.1, OCM-1, MKT-BR and of human transformed uveal melanocyte cell line UW-1. Compared to rofecoxib, nepafenac might reveal a better systemic safety profile.

In Vivo

Nepafenac shows significantly greater ocular bioavailability and amfenac demonstrated greater potency at COX-2 inhibition than ketorolac or bromfenac. Nepafenac exhibits only weak COX-1 inhibitory activity with IC50 of 64.3 mM. Nepafenac inhibits prostaglandin synthesis in the iris/ciliary body (85-95%) and the retina/choroid (55%) in rabbits. Nepafenac (0.5%) produces 65% reduction in retinal edema which is correlated with 62% inhibition of blood-retinal barrier breakdown. Nepafenac (0.5%) significantly inhibits (46%) blood-retinal barrier breakdown concomitant with near total suppression of PGE2 synthesis (96%). Nepafenac significantly inhibits retinal prostaglandin E(2), superoxide, cyclooxygenase-2, and leukostasis within retinal microvessels in insulin-deficient diabetic rats, without affecting vascular endothelial growth factor (VEGF) and nitric oxide (NO). Nepafenac significantly inhibits the number of transferase-mediated dUTP nick-end labeling-positive capillary cells, acellular capillaries, and pericyte ghosts in diabetic rats. Nepafenac results in significantly less choroidal neovascularization and significant less ischemia-induced retinal neovascularization in mice compare to control. Nepafenac also blunts the increase in VEGF mRNA in the retina induced by ischemia. Nepafenac delays the progression of malignancy as well as reduces weight in an ocular and metastatic animal model of uveal melanoma.

Animal model

Nepafenac showed to significantly decrease the retinal levels of PGE2 in LPS-induced rats when administrated topically. However, nepafenac has revealed no significant effect on BRB permeability in LPS-induced rat model

Formulation & Dosage

N/A

References

Inflammation. 2000 Aug;24(4):357-70; Inflammation. 2003 Oct;27(5):281-91; Invest Ophthalmol Vis Sci. 2003 Jan;44(1):409-15.

CAS NO:	78281-72-8
规格:	≥98%

包装	价格(元)
100mg	电议
250mg	电议
500mg	电议
1g	电议
2g	电议
5g	电议
10g	电议
25g	电议