Anecortave Acetate - CAS 7753-60-8
Catalog number: 7753-60-8
Category: Inhibitor
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Molecular Formula:
C23H30O5
Molecular Weight:
386.49
COA:
Inquire
Targets:
Others
Description:
Anecortave is a novel angiogenesis inhibitor. It can be used for the treatment of the exudative (wet) form of age-related macular degeneration. Anecortave possesses no glucocorticoid activity.
Purity:
>95%
Appearance:
Solid powder
Synonyms:
[2-[(8R,10S,13S,14R,17R)- 17-hydroxy-10,13-dimethyl-3-oxo- 2,6,7,8,12,14,15,16-octahydro- 1H-cyclopenta[a]phenanthren-17-yl]- 2-oxo-ethyl] acetate
Solubility:
Soluble in DMSO
Storage:
-20℃ Freezer
MSDS:
Inquire
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Quantity:
Milligrams-Grams
Canonical SMILES:
C(=C(/c1ccccc1)C(F)(F)F)(\c1ccc(OCCNCCO)cc1)c1ccccc1
1.Immunological factors in the pathogenesis and treatment of age-related macular degeneration.
Kijlstra A;La Heij E;Hendrikse F Ocul Immunol Inflamm. 2005 Feb;13(1):3-11.
Recent findings indicate that immunological factors are involved not only in the pathogenesis of age-related macular degeneration (AMD), but also in its treatment. Earlier data showing the presence of inflammatory cells in affected areas of AMD retinas support this statement. Although a possible role for autoimmunity was initially suggested, it has never reached general acceptance. Microorganisms have also been implied in the pathogenesis of AMD. Both serum antibacterial antibody levels and positive DNA tests from neovascular membranes have pointed to a possible role for Chlamydia pneumoniae in the pathogenesis of AMD. New data is providing evidence for the hypothesis that deposits between Bruch's membrane and the retinal pigment epithelium (RPE) cell layer may act as a stimulus for the local activation of the complement system. This may lead to a further growth of the deposits due to the strong chemotactic activity of certain complement activation products (such as C5a) with an influx of inflammatory cells. The buildup of cells and extracellular deposits may lead to local ischemia resulting in the activation of RPE cells. These activated RPE cells are thought to release angiogenic stimuli leading to choroidal neovascularization, which is the most serious complication of AMD.
2.Pharmacokinetics and metabolism of anecortave acetate in animals and humans.
Dahlin DC;Rahimy MH Surv Ophthalmol. 2007 Jan;52 Suppl 1:S49-61.
The ocular delivery of anecortave acetate was tested in preclinical and clinical pharmacokinetic and metabolism studies. Results of initial studies led to the design of a new cannula that could effectively deliver anecortave acetate as a posterior juxtascleral depot, providing adequate retinal and choroidal drug concentrations for up to 6 months after a single administration. A counter-pressure device was designed to prevent drug reflux during and immediately after posterior juxtascleral depot administration. Pharmacokinetic studies support the effectiveness of these devices. Anecortave acetate is rapidly hydrolyzed by esterases to pharmacologically active anecortave desacetate, and is further reductively metabolized to one major and several minor products that circulate as glucuronide conjugates. Low levels of these anecortave acetate metabolites were detectable for only approximately 2 weeks in the plasma after a 15-mg posterior juxtascleral depot administration to age-related macular degeneration patients. Studies show that posterior juxtascleral depot administration of anecortave acetate is an effective, minimally invasive method of delivering this drug to the choroid and retina.
3.Progressive visual loss in subfoveal exudation in age-related macular degeneration: a meta-analysis using Lineweaver-Burke plots.
Shah AR;Del Priore LV Am J Ophthalmol. 2007 Jan;143(1):83-89. Epub 2006 Oct 20.
PURPOSE: ;To analyze the randomized clinical trials in exudative age-related macular degeneration (AMD) to reveal apparent differences in the behavior of untreated control eyes among these trials. Herein we test the hypothesis that the behavior of untreated control eyes is actually the same in all studies, with apparent differences arising from differences in the time of entry of eyes into clinical trials.;DESIGN: ;Retrospective meta-analysis of prior clinical trials.;METHODS: ;Control eye data from six AMD studies (Macular Photocoagulation Study, Subfoveal Surgery Trial, Photodynamic Therapy [TAP] With Visudyne, pegaptanib trial for neovascular AMD, anecortave acetate trial, and 360 degree Macular Translocation Study) were plotted on a double reciprocal plot of 1/(Letters Lost) vs 1/(Months After Enrollment). To account for differences in time of entry into clinical trials, we introduced a horizontal translation factor to shift each data subset horizontally to maximize r(2) for the cumulative trend line.;RESULTS: ;Cumulative data for untreated control eyes fits a straight line on a double reciprocal plot (r(2) = .9521); an untreated eye would eventually deteriorate to a final vision of 20/640.
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CAS 7753-60-8 Anecortave Acetate

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