Hematoporphyrin monomethyl ether
CAS No. 148471-91-4
Hematoporphyrin monomethyl ether( —— )
Catalog No. M35081 CAS No. 148471-91-4
Hematoporphyrin monomethyl ether is a porphyrin photosensitizer that can be used in studies of port wine stains.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
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| 10MG | 187 | In Stock |
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| 25MG | 351 | In Stock |
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| 50MG | 511 | In Stock |
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| 100MG | 734 | In Stock |
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Biological Information
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Product NameHematoporphyrin monomethyl ether
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NoteResearch use only, not for human use.
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Brief DescriptionHematoporphyrin monomethyl ether is a porphyrin photosensitizer that can be used in studies of port wine stains.
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DescriptionHematoporphyrin monomethyl ether, second generation of porphyrin-related photosensitizer, is characterized by its single form, high yield of singlet oxygen, high selectivity, and low toxicity, which has been widely used in the diagnosis and research of various tumors, including lung cancer, bladder cancer, and nevus flammeus and brain glioma.
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In VitroHematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT can induce cell deaththrough both necrosis and apoptosis in HeLa cells. ROS, such as singlet oxygen and hydroxyl radical, generated in HeLa cells play a decisive role in HMME-PDT-induced cell death.
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In Vivo——
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Synonyms——
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PathwayApoptosis
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TargetApoptosis
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RecptorApoptosis
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Research Area——
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Indication——
Chemical Information
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CAS Number148471-91-4
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Formula Weight612.72
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Molecular FormulaC35H40N4O6
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Purity>98% (HPLC)
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SolubilityIn Vitro:?DMSO : 62.5 mg/mL (51.00 mM; Ultrasonic )
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SMILESCOC(C)c1c(C)c2cc3[nH]c(cc4nc(cc5[nH]c(cc1n2)c(C)c5C(C)O)c(C)c4CCC(O)=O)c(CCC(O)=O)c3C.COC(C)c1c(C)c2cc3nc(cc4[nH]c(cc5nc(cc1[nH]2)c(C)c5CCC(O)=O)c(CCC(O)=O)c4C)c(C)c3C(C)O
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Chemical Name——
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1. Ding X, et al. Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation. Cancer Lett. 2004;216(1):43-54.?
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