Name | Verteporfin |
Synonyms | Visudyne Verteprofin VERTEPIRFIN Verteporfin Verteporphin Verteporfin(DB00460) trans-3,4-Dicarboxy-4,4a-dihydro-4a,8,14,19-tetramethyl-18-vinyl-23H,25H-benzo(b)porphine-9,13-dipropionic acid 3,4,9-trimethyl ester 24H,26H-Benzo[b]porphine-9,13-dipropanoic acid, 18-ethenyl-4,4a-dihydro-3,4-bis(methoxycarbonyl)-4a,8,14,19-tetramethyl-, monomethyl ester, (4R,4aS)-rel- 9-methyl (I)13-methyl (II)trans-(±)- 18-ethenyl- 4,4a-dihydro-3,4 -bis(methoxycarbonyl)- 4a,8,14,19-tetramethyl- 23H,25H-benzo[b]porphine- 9,13- dipropanoate |
CAS | 129497-78-5 |
InChI | InChI=1/2C41H42N4O8/c1-9-23-20(2)29-17-34-27-13-10-26(39(49)52-7)38(40(50)53-8)41(27,5)35(45-34)19-30-22(4)24(11-14-36(46)47)32(44-30)18-33-25(12-15-37(48)51-6)21(3)28(43-33)16-31(23)42-29;1-9-23-20(2)29-17-34-27-13-10-26(39(49)52-7)38(40(50)53-8)41(27,5)35(45-34)19-30-22(4)25(12-15-37(48)51-6)33(44-30)18-32-24(11-14-36(46)47)21(3)28(43-32)16-31(23)42-29/h2*9-10,13,16-19,38,43,45H,1,11-12,14-15H2,2-8H3,(H,46,47)/b31-16-,32-18-,34-17-,35-19-;31-16-,33-18-,34-17-,35-19-/t2*38-,41+/m00/s1 |
InChIKey | YHNBVDZVUQFVLS-RDSGBMLISA-N |
Molecular Formula | 2C41H42N4O8 |
Molar Mass | 1437.61 |
Solubility | DMSO: soluble2mg/mL, clear (warmed) |
Appearance | powder |
Color | Black |
Storage Condition | -20°C |
Stability | Stable for 2 years from date of purchsae as supplied. Solutions in DMSO may be stored at -20°C for up to 3 months. |
In vitro study | The best wavelength for penetrating tissue (I. e., at about 700 nm), Verteporfin is about 4 times more effective than hematoporphyrin, thus providing Higher cytotoxicity than hematoporphyrin (more than 10 times in human adherent cells). Verteporfin is lipophilic and is more readily taken up by malignant or activated cells than normal or resting cells. Verteporfin binds to LDL to form a complex that is subsequently taken up by proliferating cells (e. G., neovascular endothelial cells), possibly through the LDL receptor or endocytosis. Verteporfin therapy achieves angiographic complete occlusion of the neovascular area through thrombus formation in the vascular channel, which in turn causes selective vascular endothelial injury. Verteporfin therapy selectively induced regenerative and isolated choroidal capillary occlusion without altering the covered photoreceptors or ganglion cells, as shown by light and electron microscopy. The activation of caspase-3 and caspase-9 in HL-60 cells and the cleavage of PARP map out that, in the presence of light, Verteporfin rapidly changes apoptosis, this change will be caused by the common caspase inhibitor ZVAD.fmk blocking. |
In vivo study | Verteporfin can be used for vascular visualization of choroidal vessels and CNV, which indicates rapid accumulation of photosensitizers in experimental CNV in monkeys. Verteporfin rapidly accumulates in the choroidal vasculature, RPE, and photoreceptors of established rabbit eyes. In mice, Verteporfin reached maximum tissue levels 3 hours after intravenous injection, followed by a rapid decline within 24 hours. Verteporfin is metabolized in the body to a less active form and is rapidly cleared, excreted mainly through feces and a small portion through urine. The effective selectivity of Verteporfin therapy prevents the leakage of fluorescent dyes from experimentally induced CNV in monkeys. |
WGK Germany | 3 |
HS Code | 2933997500 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 0.696 ml | 3.478 ml | 6.956 ml |
5 mM | 0.139 ml | 0.696 ml | 1.391 ml |
10 mM | 0.07 ml | 0.348 ml | 0.696 ml |
5 mM | 0.014 ml | 0.07 ml | 0.139 ml |