| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg | |||
| Other Sizes |
| Targets |
Redaporfin targets cancer cells through photodynamic therapy (PDT). Upon activation by near-infrared light, Redaporfin produces reactive oxygen species (ROS), including singlet oxygen. These ROS induce oxidative stress, leading to the destruction of cancer cells through apoptosis and necrosis. Redaporfin preferentially accumulates in proliferative tissues such as tumors. The combination of PDT with Redaporfin induces a reduction in the abundance of several Golgi apparatus proteins.
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| ln Vitro |
The Golgi apparatus (GA) proteins, eukaryotic translation initiation factor 2-alpha (eIF2α) kinase 3 (EIF2AK3) and protein Disulfide isomerase A3 (PDIA3), as well as Golkin subfamily A member 2 (GOLGA2), galactosyltransferase 1 (GALT1), and several other GA proteins are reduced in abundance when photodynamic therapy (PDT) combined with redaporfin (5μM) is applied. Conversely, there was no discernible decrease in the cytoskeletal protein β-actin or the mitochondrial import receptor component TOM20 homolog (TOMM20) [1].
In vitro, Redaporfin is a potent photosensitizer with direct anti-tumor activities. When activated by light, it produces ROS that can kill cancer cells. The combination of photodynamic therapy (PDT) with Redaporfin (5 μM) induces a reduction in the abundance of several Golgi apparatus (GA) proteins. These in vitro studies confirm Redaporfin's activity as a photosensitizer and its ability to induce cancer cell death upon light activation. |
| ln Vivo |
In vivo, Redaporfin has shown high efficacy in the treatment of male BALB/c mice with subcutaneously implanted colon (CT26) tumors. Vascular-PDT with 1.5 mg/kg Redaporfin and a light dose of 74 J/cm² led to complete tumor regression in 83% of the mice. A proof-of-concept clinical trial has shown promising results in the treatment of advanced head and neck cancer. The compound was reported to be safe, well-tolerated, and effective.
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| Enzyme Assay |
In vitro assays for Redaporfin measure its photosensitizing activity. The compound is incubated with cells or with a model system (e.g., a solution containing a singlet oxygen sensor) and irradiated with near-infrared light. The production of reactive oxygen species is measured using fluorescent probes or by assessing the oxidation of a substrate. The cytotoxicity of photoactivated Redaporfin is assessed using cell viability assays. These assays confirm the compound's activity as a photosensitizer.
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| Cell Assay |
Western Blot Analysis [1]
Cell Types: Human osteosarcoma U2OS cells Tested Concentrations: 0.3, 0.6, 1.3, 2.5, 5, 10 μM Incubation Duration: 6 hrs (hours) Experimental Results: Induced GBF1, GOLGA2 and GALT1 abundance diminished such as EIF2AK3 and PDIA3. In vitro cell-based assays for Redaporfin are used to study its photodynamic therapy (PDT) effects on cancer cells. Cancer cells are treated with Redaporfin at various concentrations, then irradiated with near-infrared light. Cell viability is assessed using assays such as MTT or CellTiter-Glo. Apoptosis is measured using Annexin V staining or caspase-3/7 activation assays. The production of ROS is measured using fluorescent probes. These assays confirm the compound's photocytotoxic activity. |
| Animal Protocol |
In vivo animal experiments for Redaporfin have been conducted in mouse models of cancer. In a typical study, BALB/c mice with subcutaneously implanted colon (CT26) tumors are treated with Redaporfin (1.5 mg/kg) and then irradiated with near-infrared light (74 J/cm²). Tumor growth is monitored, and complete tumor regression is observed in 83% of treated mice. These studies provide evidence for the in vivo efficacy of Redaporfin in PDT.
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| ADME/Pharmacokinetics |
Redaporfin has a molecular weight not specified in standard product descriptions. It is a porphyrin-based compound. It is a solid compound. It is soluble in DMSO and other organic solvents. For storage, it is recommended to keep the powder at -20°C. Detailed pharmacokinetic properties such as absorption, distribution, metabolism, and excretion (ADME) have been characterized in preclinical and clinical studies. Redaporfin is administered intravenously and preferentially accumulates in tumors.
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| Toxicity/Toxicokinetics |
Detailed toxicity data for Redaporfin is available from its clinical development. In a proof-of-concept clinical trial, the compound was reported to be safe and well-tolerated by patients. As a photosensitizer, it can cause skin photosensitivity, and patients are advised to avoid light exposure after treatment. Specific toxicity data, such as adverse effects or organ toxicity, are not detailed in standard product descriptions. As with all research chemicals, standard laboratory safety precautions should be followed.
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| References | |
| Additional Infomation |
Redapoxetine is a chlorophyll-based photosensitizer with antitumor activity in photodynamic therapy (PDT). After intravenous injection, redapoxetine preferentially accumulates in proliferative tissues such as tumors. Local laser irradiation at the tumor site allows redapoxetine to absorb light energy, triggering a photodynamic reaction between LUZ 11 and oxygen. This reaction generates reactive oxygen species (ROS), including singlet oxygen molecules, superoxide anions, and other cytotoxic free radicals. ROS generation induces free radical-mediated DNA damage and cell death.
Redaporfin is a research compound and is not approved for clinical use. It is a photosensitizer used in photodynamic therapy (PDT) for cancer treatment. It is a porphyrin-based compound that, when activated by near-infrared light, produces reactive oxygen species, leading to the destruction of cancer cells. Redaporfin has shown high efficacy in the treatment of colon tumors in mice and promising results in a proof-of-concept clinical trial for advanced head and neck cancer. It is a valuable research tool for studying PDT. |
| Exact Mass |
1134.156
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| CAS # |
1224104-08-8
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| PubChem CID |
86287614
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| Appearance |
Brown to black solid powder
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| Density |
1.5±0.1 g/cm3
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| Index of Refraction |
1.617
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| LogP |
11.24
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| Hydrogen Bond Donor Count |
6
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| Hydrogen Bond Acceptor Count |
22
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| Rotatable Bond Count |
12
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| Heavy Atom Count |
76
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| Complexity |
2150
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| Defined Atom Stereocenter Count |
0
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| SMILES |
S(C1C([H])=C([H])C(=C(C=1F)C1=C2C([H])=C([H])C(=C(C3=C(C([H])=C([H])C(=C3F)S(N([H])C([H])([H])[H])(=O)=O)F)C3C([H])([H])C([H])([H])C(=C(C4=C(C([H])=C([H])C(=C4F)S(N([H])C([H])([H])[H])(=O)=O)F)C4=C([H])C([H])=C(C(C5=C(C([H])=C([H])C(=C5F)S(N([H])C([H])([H])[H])(=O)=O)F)=C5C([H])([H])C([H])([H])C1=N5)N4[H])N=3)N2[H])F)(N([H])C([H])([H])[H])(=O)=O |c:11,17,46,t:94|
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| InChi Key |
CKRVBMUJCFKRND-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C48H38F8N8O8S4/c1-57-73(65,66)33-17-5-21(49)37(45(33)53)41-25-9-11-27(61-25)42(38-22(50)6-18-34(46(38)54)74(67,68)58-2)29-13-15-31(63-29)44(40-24(52)8-20-36(48(40)56)76(71,72)60-4)32-16-14-30(64-32)43(28-12-10-26(41)62-28)39-23(51)7-19-35(47(39)55)75(69,70)59-3/h5-9,11,14,16-20,57-61,64H,10,12-13,15H2,1-4H3
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| Chemical Name |
2,4-difluoro-N-methyl-3-[10,15,20-tris[2,6-difluoro-3-(methylsulfamoyl)phenyl]-2,3,12,13,22,24-hexahydroporphyrin-5-yl]benzenesulfonamide
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| Synonyms |
F2BMet LUZ 11 LUZ11F-2BMet LUZ-11 F 2BMet
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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 |
| 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 : ~100 mg/mL (~88.10 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 6.25 mg/mL (5.51 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 62.5 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: ≥ 6.25 mg/mL (5.51 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in 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 62.5 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 6.25 mg/mL (5.51 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT02070432 | UNKNOWN STATUS | Drug: LUZ11 | Head and Neck Cancer | Luzitin SA | 2014-02 | Phase 1 Phase 2 |
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