product name Verteporfin
Description: Verteporfin, also known as Benzoporphyrin derivative monoacid ring A or BPD-MA, is a potent second-generation photosensitizing agent derived from porphyrin in endothelial cells. Verteporfin is a benzoporphyrin derivative and is a medication used as a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as the wet form of macular degeneration. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 693 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals.
References: Surv Ophthalmol. 2000 Nov-Dec;45(3):195-214; Blood. 2000 Jan 1;95(1):256-62.
718.79
Formula
C41H42N4O8
CAS No.
129497-78-5
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (139.1 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
CL 318952, BPD-MA
other peoduct :
| In Vitro |
In vitro activity: Verteporfin is about four times more efficient in absorbing light at wavelengths that penetrate tissues best (i.e., around 700 nm) and thus provides a much higher cytotoxic effect than hematoporphyrin (10 times more in human adherent cell lines). Verteporfin is lipophilic and is more readily taken up by malignant or activated cells, compared with normal or resting cells. Verteporfin binds with LDL to form a complex, which is then taken up into proliferating cells (e.g., neovascular endothelial cells) probably via LDL receptors and endocytosis. Verteporfin therapy achieves complete angiographic occlusion of the neovascular compartment by thrombosis of vascular channels, following selective endothelial damage. Verteporfin therapy selectively induces reproducible and isolated choriocapillary occlusion without alteration of overlying photoreceptors or ganglion cells, as shown by light and electron microscopy. Verteporfin conbined with light rapidly exhibits apoptotic changes reflected by caspase-3 and caspase-9 activation and PARP cleavage in HL-60 cells, changes that are blocked by the general caspase inhibitor ZVAD.fmk. Kinase Assay: Cell Assay: |
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| In Vivo | Verteporfin can be used for angiographic visualization of choroidal vessels and CNV, which demonstrates that the photosensitizer accumulates rapidly in experimental CNV in monkeys. Verteporfin accumulates rapidly in the established vasculature of the choroid, RPE, and photoreceptors of rabbit eyes. Verteporfin reaches maximal tissue levels within 3 hours of intravenous injection, followed by a rapid decline within 24 hours in mice. Verteporfin is metabolized to a less active form in vivo and is cleared very rapidly, predominantly in the feces and a very small proportion excreted in urine. Verteporfin therapy effectively and selectively prevents fluorescein dye leakage from experimentally induced CNV in monkeys. |
| Animal model | |
| Formulation & Dosage | |
| References | Surv Ophthalmol. 2000 Nov-Dec;45(3):195-214; Blood. 2000 Jan 1;95(1):256-62. |
