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| ln Vitro |
Pyropheophorbide-a (PPa) exhibits photodynamic cytotoxicity against tumor cells. In human cervical cancer HeLa cells, under 660 nm laser irradiation (1 J/cm²), it induced concentration-dependent cell death with an IC50 of 0.8 μM. At 2 μM, apoptotic rate reached 68% (Annexin V-FITC/PI staining), accompanied by a 3.2-fold increase in reactive oxygen species (ROS) production compared to control [4]
In cRGD-conjugated form (cRGD-PPa), it showed enhanced targeting to U87MG glioblastoma cells (overexpressing integrin αvβ3). Under 660 nm irradiation (2 J/cm²), cRGD-PPa (1 μM) induced 82% cell death, while free PPa only caused 45% cell death at the same concentration. It also accumulated more efficiently in U87MG cells (fluorescence intensity 3.5-fold higher than free PPa) [1] In 3T3-L1 preadipocytes, Pyropheophorbide-a (PPa) (5-20 μM) exerted anti-adipogenic activity. At 20 μM, it reduced lipid accumulation by 72% (Oil Red O staining) and downregulated adipogenic transcription factors: PPARγ mRNA expression by 60%, C/EBPα by 55%, and FABP4 by 68% (qPCR). It also inhibited intracellular triglyceride (TG) synthesis (48% reduction at 20 μM) without affecting cell viability (>90% at 20 μM) [2] In human retinal pigment epithelial (RPE) cells (ARPE-19), Pyropheophorbide-a (PPa) (0.1-1 μM) showed photodynamic activity under 660 nm irradiation (0.5 J/cm²). At 1 μM, it induced 75% death of abnormally proliferating ARPE-19 cells, with minimal toxicity to normal RPE cells (viability >85% at 1 μM) [3] |
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| ln Vivo |
In nude mice bearing U87MG glioblastoma xenografts (n=6 per group), intravenous injection of cRGD-PPa (5 mg/kg) followed by 660 nm laser irradiation (100 mW/cm², 10 minutes) every 3 days for 2 weeks significantly inhibited tumor growth. Tumor volume was reduced by 78% compared to the saline control group, and tumor weight was decreased by 72%. Fluorescence imaging showed strong accumulation of cRGD-PPa in tumors (signal 4.3-fold higher than free PPa) at 24 hours post-administration [1]
In rats with sodium iodate-induced age-related macular degeneration (AMD) (n=8 per group), intravitreal injection of Pyropheophorbide-a (PPa) (0.2 μg/eye) followed by 660 nm laser irradiation (0.3 J/cm²) improved retinal function. Electroretinogram (ERG) analysis showed that the b-wave amplitude increased by 56% compared to the model group. Histological examination revealed reduced RPE cell loss (by 63%) and choroidal neovascularization (CNV) area (by 58%) [3] |
| Cell Assay |
HeLa cell phototoxicity assay: HeLa cells were cultured in DMEM with fetal bovine serum, seeded in 96-well plates (1×10⁴ cells/well), and incubated with Pyropheophorbide-a (PPa) (0.1-5 μM) for 24 hours. Cells were irradiated with 660 nm laser (1 J/cm²), then cultured for another 24 hours. Cell viability was measured by MTT assay; apoptosis by Annexin V-FITC/PI staining; ROS production by DCFH-DA staining [4]
3T3-L1 adipogenesis inhibition assay: 3T3-L1 preadipocytes were seeded in 24-well plates (5×10³ cells/well), cultured to confluence, then induced to differentiate with adipogenic medium. Pyropheophorbide-a (PPa) (5-20 μM) was added during differentiation. After 8 days, cells were stained with Oil Red O to quantify lipid accumulation; TG content was measured by enzymatic kit; adipogenic gene expression by qPCR [2] U87MG cell targeting and cytotoxicity assay: U87MG cells were seeded in 6-well plates (2×10⁵ cells/well), incubated with cRGD-PPa or free Pyropheophorbide-a (PPa) (1 μM) for 4 hours. Cellular uptake was observed by fluorescence microscopy. For cytotoxicity, cells were irradiated with 660 nm laser (2 J/cm²) after incubation, cultured for 24 hours, and viability was assessed by MTT assay [1] ARPE-19 cell photodynamic assay: ARPE-19 cells were seeded in 96-well plates (8×10³ cells/well), treated with Pyropheophorbide-a (PPa) (0.1-1 μM) for 12 hours, irradiated with 660 nm laser (0.5 J/cm²), and cultured for 48 hours. Cell viability was measured by CCK-8 assay; RPE cell function by rhodopsin expression detection [3] |
| Animal Protocol |
Nude mouse tumor xenograft model: Female BALB/c nude mice (4-6 weeks old) were subcutaneously inoculated with U87MG cells (5×10⁶ cells/mouse). When tumors reached 100 mm³, mice were randomly divided into control, free PPa, and cRGD-PPa groups (n=6 per group). Pyropheophorbide-a (PPa) or cRGD-PPa was dissolved in 10% DMSO + 90% saline (5 mg/mL) and administered via tail vein injection (5 mg/kg). After 24 hours, tumors were irradiated with 660 nm laser (100 mW/cm², 10 minutes). The treatment was repeated every 3 days for 2 weeks. Tumor volume was measured every 2 days; mice were euthanized at the end to weigh tumors and detect tissue distribution by fluorescence imaging [1]
Rat AMD model: Male Sprague-Dawley rats (200-250 g) were intravenously injected with sodium iodate (50 mg/kg) to induce AMD. One week later, rats were divided into model and treatment groups (n=8 per group). Pyropheophorbide-a (PPa) was dissolved in sterile phosphate-buffered saline (0.02 μg/μL) and administered via intravitreal injection (0.2 μg/eye). After 4 hours, rats were irradiated with 660 nm laser (0.3 J/cm²) around the macula. Four weeks later, ERG was performed to assess retinal function; eyes were enucleated for histological analysis and CNV area measurement [3] |
| Toxicity/Toxicokinetics |
In vitro toxicity: Pyropheophorbide a (PPa) (at concentrations up to 20 μM) did not show significant cytotoxicity to unirradiated 3T3-L1 preadipocytes (MTT assay: cell viability >92%) [2] In ARPE-19 cells, unirradiated pyromethophylate a (PPa) (at concentrations up to 1 μM) did not affect cell viability (cell viability >90%) [3] In nude mice, intravenous injection of cRGD-PPa (5 mg/kg) for 2 weeks did not cause significant changes in body weight, liver function (ALT/AST), or kidney function (creatinine/BUN). No histopathological abnormalities were observed in the liver, kidneys, heart, or lungs [1] In AMD model rats, intravitreal injection of pyromethophylate a (PPa) (0.2 μg/eye) did not cause retinal inflammation or structural damage (H&E staining), and serum toxicological parameters were within the normal range [3]
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| References |
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| Additional Infomation |
Pyropheophorbide is a pheophylate. It is the conjugate acid of the pyromethophylate a anion. Pyropheophorbide a has been reported to exist in the water scallop (Mizuhopecten yessoensis), the monophylla scallop (Atalantia monophylla), and other organisms with relevant data. Pyropheophorbide a (PPa) is a natural chlorophyll-derived photosensitizer that can be isolated from sources such as wild bitter melon (Momordica charantia L. var. abbreviata Seringe)[2]. Its photodynamic therapy (PDT) mechanism involves the generation of reactive oxygen species (ROS, including singlet oxygen and superoxide anion) under 660 nm near-infrared light irradiation, thereby inducing oxidative stress and apoptosis in target cells[1][3][4].
Binding with cRGD peptide can enhance its targeting of tumor cells overexpressing integrin αvβ3, improve tumor selective accumulation and reduce off-target toxicity[1] Its anti-adipogenesis mechanism is mediated by downregulating key adipogenesis transcription factors (PPARγ, C/EBPα) and lipid synthesis-related genes (FABP4), inhibiting preadipocyte differentiation into mature adipocytes[2] It has potential application value in photodynamic therapy for tumors and age-related macular degeneration as well as in anti-obesity research[1][2][3][4]. |
| Molecular Formula |
C₃₃H₃₄N₄O₃
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|---|---|
| Molecular Weight |
534.65
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| Exact Mass |
534.263
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| CAS # |
24533-72-0
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| PubChem CID |
161456
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| Appearance |
Brown to black solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
991.5±65.0 °C at 760 mmHg
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| Flash Point |
553.5±34.3 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.665
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| LogP |
6.49
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
40
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| Complexity |
1660
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| Defined Atom Stereocenter Count |
2
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| SMILES |
CCC1=C(C2=NC1=CC3=C(C4=C(CC(=C5[C@H]([C@@H](C(=CC6=NC(=C2)C(=C6C)C=C)N5)C)CCC(=O)O)C4=N3)O)C)C
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| InChi Key |
FDKRLXBXYZKWRZ-UWJYYQICSA-N
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| InChi Code |
InChI=1S/C33H34N4O3/c1-7-19-15(3)23-12-25-17(5)21(9-10-30(39)40)32(36-25)22-11-29(38)31-18(6)26(37-33(22)31)14-28-20(8-2)16(4)24(35-28)13-27(19)34-23/h7,12-14,17,21,36,38H,1,8-11H2,2-6H3,(H,39,40)/t17-,21-/m0/s1
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| Chemical Name |
3-[(21S,22S)-16-ethenyl-11-ethyl-4-hydroxy-12,17,21,26-tetramethyl-7,23,24,25-tetrazahexacyclo[18.2.1.15,8.110,13.115,18.02,6]hexacosa-1,4,6,8(26),9,11,13(25),14,16,18(24),19-undecaen-22-yl]propanoic acid
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~12.5 mg/mL (~23.38 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.25 mg/mL (2.34 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 1.25 mg/mL (2.34 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.8704 mL | 9.3519 mL | 18.7038 mL | |
| 5 mM | 0.3741 mL | 1.8704 mL | 3.7408 mL | |
| 10 mM | 0.1870 mL | 0.9352 mL | 1.8704 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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