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Verteporfin

  • 產(chǎn)品貨號:CS-01Y73843
  • 產(chǎn)品價格:電議
  • 產(chǎn)品產(chǎn)地:進口、國產(chǎn)
  • 包裝類型:10mM (in 1mL DMSO) 5mg 25mg
  • 采購熱度:209
  • 庫存:100
  • CAS號:129497-78-5
  • 方法:
  • 含量:>98.00%
  • 品牌名稱:莼試
  • 分子式:C41H42N4O8
  • 分子量:718.79

簡介內(nèi)容:質(zhì)量保證、價格優(yōu)惠

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標簽:Verteporfin 

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規(guī)格

10mM (in 1mL DMSO) 5mg 25mg

CAS

129497-78-5

別名

CL 318952;Visudyne

化學(xué)名

 

分子式

C41H42N4O8

分子量

718.79

溶解度

18.3mg/mL in DMSO

儲存條件

4°C, protect from light

General tips

For obtaining a higher solubility , please warm the tube at 37 and shake it in the ultrasonic bath for a while.

Shipping Condition

Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

 

產(chǎn)品描述:                                                                                                            

Verteporfin, derived from porphyrin, is a potent photosensitizing agent, which has all the features theoretically necessary for effective photodynamic therapy (PDT) in ocular neovascularization [1].

Experimentas showed that the mechanism of action of verteporfin therapy is intravascular damage leading to the formation of thrombus and selective vascular occlusion. Photodynamic therapy with verteporfin triggers cellular events consistent with a number of the changes described for cells rendered by different chemotherapeutic agents.

More than 90% of HL-60 cells treated with verteporfin at 100 ng/mL showed a hypodiploid level of DNA, when approximately 25% of irradiated cells treated with verteporfin at 50 ng/mL exhibited DNA fragmentation. For cells treated with verteporfin at 25 ng/mL, there was an 85% or greater loss in viability as determined by MTT assays performed 24 hours after irradiation. A 5–6 hours of the plasma half-life of verteporfin was shown in a pharmacokinetic studies in humans. At 6 mg/m2, which is the clinically relevant dose being used in neovascular AMD, no skin photosensitivity was detected at 24 hours, whereas at 18 mg/m2, baseline was reached by 5 days [1, 2].

Verteporfin was also found to inhibit autophagosome formation that does not require exposure to light. Verteporfin could target and modify p62 directly, a protein of scaffold and adaptor that binds both polyubiquitinated proteins destined for degradation and LC3 on autophagosomal membranes. Co-immunoprecipitation experiments demonstrated that crosslinked p62 oligomers retain their ability to bind to LC3 but show defective binding to polyubiquitinated proteins. Interestingly, small amounts of crosslinked p62 oligomers were detected in cells which were untreated, and other groups which were noted the accumulation of p62 forms with reduced SDS-PAGE mobility in cellular and animal models of oxidative stress and aging [3].

特別提醒:                                                                                                              

1. 本產(chǎn)品僅供科研使用。請勿用于醫(yī)藥、臨床診斷或治療,食品及化妝品等用途。請勿存放于普通住宅區(qū)。

2. 為了您的安全和健康,請穿好實驗服并佩戴一次性手套和口罩操作。

原創(chuàng)作者:上海莼試生物技術(shù)有限公司

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