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MedKoo Cat#: 203120 | Name: Verteporfin
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Description:

WARNING: This product is for research use only, not for human or veterinary use.

Verteporfin, also known as Benzoporphyrin derivative monoacid ring A or BPD-MA, 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, resulting in local damage to the endothelium and blockage of the vessels. Verteporfin is also used off-label for the treatment of central serous retinopathy.

Chemical Structure

Verteporfin
Verteporfin
CAS#129497-78-5

Theoretical Analysis

MedKoo Cat#: 203120

Name: Verteporfin

CAS#: 129497-78-5

Chemical Formula: C41H42N4O8

Exact Mass: 718.3003

Molecular Weight: 718.79

Elemental Analysis: C, 68.51; H, 5.89; N, 7.79; O, 17.81

Price and Availability

Size Price Availability Quantity
5mg USD 90.00 Ready to ship
10mg USD 150.00 Ready to ship
25mg USD 250.00 Ready to ship
50mg USD 450.00 Ready to ship
100mg USD 750.00 Ready to ship
200mg USD 1,350.00 Ready to ship
500mg USD 2,950.00 Ready to ship
1g USD 5,250.00 Ready to ship
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Related CAS #
No Data
Synonym
DB00460, CL 318952, BPD-MA, BpdMA, Benzoporphyrin D, Benzoporphyrin derivative monoacid ring A, Verteporfin, Visudyne.
IUPAC/Chemical Name
(1): 3-[(23S,24R)-14-ethenyl-5-(3-methoxy-3-oxopropyl)-22,23-bis(methoxycarbonyl)-4,10,15,24-tetramethyl-25,26,27,28-tetraazahexacyclo[16.6.1.13,6.18,11.113,16.019,24]octacosa-1,3,5,7,9,11(27),12,14,16,18(25),19,21-dodecaen-9-yl]propanoic acid.
InChi Key
YTZALCGQUPRCGW-MXVXOLGGSA-N
InChi Code
InChI=1S/C41H42N4O8/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)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/h9-10,13,16-19,38,42,44H,1,11-12,14-15H2,2-8H3,(H,46,47)/b28-16-,29-17-,30-19-,31-16-,32-18-,33-18-,34-17-,35-19-/t38-,41+/m0/s1
SMILES Code
O=C(O)CCC1=C(C)C(/C=C2C(C=C)=C(C)/C(N/2)=C/3)=N/C1=C\C(N4)=C(CCC(OC)=O)C(C)=C4/C=C5[C@]6(C)[C@H](C(OC)=O)C(C(OC)=O)=CC=C6C3=N/5.
Appearance
Black solid powder
Purity
>95% (or refer to the Certificate of Analysis)
Shipping Condition
Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.
Storage Condition
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).
Solubility
Soluble in DMSO, not in water
Shelf Life
>2 years if stored properly
Drug Formulation
This drug may be formulated in DMSO
Stock Solution Storage
0 - 4 C for short term (days to weeks), or -20 C for long term (months).
HS Tariff Code
2934.99.9001
More Info
Verteporfin is A synthetic light-activated agent with photodynamic activity. Upon systemic administration, verteporfin accumulates in neovessels in the eye and, once stimulated by nonthermal red light in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to neovascular endothelium and blood vessel occlusion. (From NCI's webpages).   DRUG DESCRIPTION VISUDYNE® (verteporfin for injection) is a light activated drug used in photodynamic therapy. The finished drug product is a lyophilized dark green cake. Verteporfin is a 1:1 mixture of two regioisomers (I and II) The chemical names for the verteporfin regioisomers are: 9-methyl (I) and 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. The molecular formula is C41H42N4O8 with a molecular weight of approximately 718.8. Each mL of reconstituted VISUDYNE contains:  ACTIVE: Verteporfin, 2 mg. INACTIVES: Lactose, egg phosphatidylglycerol, dimyristoyl phosphatidylcholine, ascorbyl palmitate and butylated hydroxytoluene   INDICATIONS VISUDYNE (verteporfin for injection) therapy is indicated for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis. There is insufficient evidence to indicate VISUDYNE for the treatment of predominantly occult subfoveal choroidal neovascularization.   Mechanism of Action VISUDYNE (verteporfin for injection) therapy is a two-stage process requiring administration of both verteporfin for injection and nonthermal red light. Verteporfin is transported in the plasma primarily by lipoproteins. Once verteporfin is activated by light in the presence of oxygen, highly reactive, short-lived singlet oxygen and reactive oxygen radicals are generated. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. Therefore, there may be collateral damage to retinal structures following photoactivation including the retinal pigmented epithelium and outer nuclear layer of the retina. The temporary occlusion of choroidal neovascularization (CNV) following Visudyne therapy has been confirmed in humans by fluorescein angiography.  
Biological target:
Verteporfin (CL 318952, Visudyne) is a small molecule that inhibits TEAD–YAP association and YAP-induced liver overgrowth.
In vitro activity:
Verteporfin suppressed PD-L1 expression effectively in all 6 cell lines (T cell leukemia; B cell leukemia; ovarian; endometrium n=3) (Fig. 1A, Supplemental Table 1, Supplemental Fig. S1). In an additional panel of 8 human cancer cell lines (ovarian, n=5; osteoblastoma, n=1; and lung cancers, n=2) and 2 murine cancer cell lines (ovarian and lung), verteporfin abolished basal PD-L1 protein expression, including differential glycosylated states as reflected by the double bands on Western Blots, regardless of genetic background, lineage specificity, and basal (intrinsic) PD-L1 levels (Fig. 1A-D). Cell fractionation revealed that verteporfin decreased membrane-associated PD-L1 (functionally relevant PD-L1) in EFE184 cells (endometrial cancer) (Fig. 1E) and flow cytometry showed that verteporfin reduced PD-L1 expression on both the surface of cancer cells (Fig. 1F) and on antigen presenting cells (Supplementary Fig. S1D). Verteporfin suppressed both IFN-induced PD-L1 protein expression (Supplemental Fig. S1B, C, D) and mRNA expression (Fig. 1G). However, in contrast to the marked loss of PD-L1 protein, verteporfin had little effect on intrinsic PD-L1 mRNA expression in the absence of IFN-γ (Fig. 1H). Thus, verteporfin engages at least two independent mechanisms to down-regulate PD-L1 expression. Reference: Cancer Immunol Res. 2020 Jul;8(7):952-965. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8204534/
In vivo activity:
The in vivo therapeutic effects of verteporfin were tested in established immune competent mice bearing ID8 cells intraperitoneally (Fig. 6B). Verteporfin had a modest effect on the survival of ID8-burdened mice. In contrast, the combination of verteporfin and BMN 673 produced a statistically significant improved outcome compared to either monotherapy that was equivalent to the combination of anti-PD-L1 and BMN 673 (Fig. 6B). In LLC (Lewis lung carcinoma) tumors for which tumors could be harvested for immune analysis, verteporfin treatment led to marked decreases in PD-L1 expression and increases in CD8 T cells especially in the combinatorial group of vereporfin and BMN 673 (Fig. 6E, D; Supplemental Fig. S6A, B). Reference: Cancer Immunol Res. 2020 Jul;8(7):952-965. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8204534/
Solvent mg/mL mM
Solubility
DMSO 70.0 97.38
DMF 20.0 27.82
Water 0.0 0.01
Note: There can be variations in solubility for the same chemical from different vendors or different batches from the same vendor. The following factors can affect the solubility of the same chemical: solvent used for crystallization, residual solvent content, polymorphism, salt versus free form, degree of hydration, solvent temperature. Please use the solubility data as a reference only. Warming and sonication will facilitate dissolving. Still have questions? Please contact our Technical Support scientists.

Preparing Stock Solutions

The following data is based on the product molecular weight 718.79 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL
Formulation protocol:
1. Liang J, Wang L, Wang C, Shen J, Su B, Marisetty AL, Fang D, Kassab C, Jeong KJ, Zhao W, Lu Y, Jain AK, Zhou Z, Liang H, Sun SC, Lu C, Xu ZX, Yu Q, Shao S, Chen X, Gao M, Claret FX, Ding Z, Chen J, Chen P, Barton MC, Peng G, Mills GB, Heimberger AB. Verteporfin Inhibits PD-L1 through Autophagy and the STAT1-IRF1-TRIM28 Signaling Axis, Exerting Antitumor Efficacy. Cancer Immunol Res. 2020 Jul;8(7):952-965. doi: 10.1158/2326-6066.CIR-19-0159. Epub 2020 Apr 7. PMID: 32265228; PMCID: PMC8204534. 2. Wang Y, Wang L, Wise JTF, Shi X, Chen Z. Verteporfin inhibits lipopolysaccharide-induced inflammation by multiple functions in RAW 264.7 cells. Toxicol Appl Pharmacol. 2020 Jan 15;387:114852. doi: 10.1016/j.taap.2019.114852. Epub 2019 Dec 5. PMID: 31812773.
In vitro protocol:
1. Liang J, Wang L, Wang C, Shen J, Su B, Marisetty AL, Fang D, Kassab C, Jeong KJ, Zhao W, Lu Y, Jain AK, Zhou Z, Liang H, Sun SC, Lu C, Xu ZX, Yu Q, Shao S, Chen X, Gao M, Claret FX, Ding Z, Chen J, Chen P, Barton MC, Peng G, Mills GB, Heimberger AB. Verteporfin Inhibits PD-L1 through Autophagy and the STAT1-IRF1-TRIM28 Signaling Axis, Exerting Antitumor Efficacy. Cancer Immunol Res. 2020 Jul;8(7):952-965. doi: 10.1158/2326-6066.CIR-19-0159. Epub 2020 Apr 7. PMID: 32265228; PMCID: PMC8204534. 2. Wang Y, Wang L, Wise JTF, Shi X, Chen Z. Verteporfin inhibits lipopolysaccharide-induced inflammation by multiple functions in RAW 264.7 cells. Toxicol Appl Pharmacol. 2020 Jan 15;387:114852. doi: 10.1016/j.taap.2019.114852. Epub 2019 Dec 5. PMID: 31812773.
In vivo protocol:
1. Liang J, Wang L, Wang C, Shen J, Su B, Marisetty AL, Fang D, Kassab C, Jeong KJ, Zhao W, Lu Y, Jain AK, Zhou Z, Liang H, Sun SC, Lu C, Xu ZX, Yu Q, Shao S, Chen X, Gao M, Claret FX, Ding Z, Chen J, Chen P, Barton MC, Peng G, Mills GB, Heimberger AB. Verteporfin Inhibits PD-L1 through Autophagy and the STAT1-IRF1-TRIM28 Signaling Axis, Exerting Antitumor Efficacy. Cancer Immunol Res. 2020 Jul;8(7):952-965. doi: 10.1158/2326-6066.CIR-19-0159. Epub 2020 Apr 7. PMID: 32265228; PMCID: PMC8204534.
1: Tan Q, Xiang C, Zhang H, Yuan Y, Gong S, Zheng Z, Wang X, Liu X, Chen Y, Tan C. YAP promotes fibrosis by regulating macrophage to myofibroblast transdifferentiation and M2 polarization in chronic pancreatitis. Int Immunopharmacol. 2025 Jan 15;148:114087. doi: 10.1016/j.intimp.2025.114087. Epub ahead of print. PMID: 39818090. 2: More CCB, Bueno AC, Rojas CAO, Stecchini MF, Ramalho FS, Brandalise SR, Cardinalli IA, Yunes JA, Junqueira T, Scrideli CA, Castro M, Antonini SRR. YAP1 is a prognostic marker and its inhibition reduces tumor progression in adrenocortical tumors. J Clin Endocrinol Metab. 2025 Jan 10:dgaf013. doi: 10.1210/clinem/dgaf013. Epub ahead of print. PMID: 39788148. 3: Drugs for age-related macular degeneration. Med Lett Drugs Ther. 2025 Jan 6;67(1719):1-5. doi: 10.58347/tml.2025.1719a. PMID: 39787576. 4: Jiang D, Li J, Ma H, Yan B, Lei H. Doublecortin-like kinase 1 promotes stem cell-like properties through the Hippo-YAP pathway in prostate cancer. Int J Med Sci. 2025 Jan 1;22(2):460-472. doi: 10.7150/ijms.99062. PMID: 39781521; PMCID: PMC11704687. 5: Shan AP, Hlaing KS, Leelahavanichkul A, Amornphimoltham P. Efficacy of metformin and verteporfin treatment alone or in combination in a murine head and neck cancer xenograft model. Eur J Oral Sci. 2025 Jan 8:e13034. doi: 10.1111/eos.13034. Epub ahead of print. PMID: 39780329. 6: Lim WY, Lee JH, Choi Y, Yoon K. Corrigendum to "Verteporfin is an effective inhibitor of HCMV replication" [Virus Research (2024) 1-5/199475]. Virus Res. 2025 Jan;351:199523. doi: 10.1016/j.virusres.2024.199523. Epub 2025 Jan 3. Erratum for: Virus Res. 2024 Dec;350:199475. doi: 10.1016/j.virusres.2024.199475. PMID: 39753384. 7: Deng J, Zhang YN, Bai RS, Yu TT, Zhao Y, Liu H, Zhang YF, Xu TM, Han B. Mechanosensor YAP mediates bone remodeling via NF-κB p65 induced osteoclastogenesis during orthodontic tooth movement. Prog Orthod. 2025 Jan 2;26(1):2. doi: 10.1186/s40510-024-00548-w. PMID: 39747791; PMCID: PMC11695529. 8: Luo X, Yang J, Zhao Y, Nagayasu T, Chen J, Hu P, He Z, Li Z, Wu J, Zhao Z, Duan G, Sun X, Zhao L, Pan Y, Wang X. Engineering spatially-confined conduits to tune nerve self-organization and allodynic responses via YAP-mediated mechanotransduction. Nat Commun. 2025 Jan 2;16(1):66. doi: 10.1038/s41467-024-55118-9. PMID: 39746959; PMCID: PMC11695937. 9: Zhang X, Liu H, Wan C, Li Y, Ren C, Lu J, Liu Y, Yang Y. Corrigendum to "Verteporfin combined with ROCK inhibitor promotes the restoration of corneal endothelial cell dysfunction in rats" [Biochem. Pharmacol. 231 (2025) 116641]. Biochem Pharmacol. 2024 Dec 31;232:116737. doi: 10.1016/j.bcp.2024.116737. Epub ahead of print. Erratum for: Biochem Pharmacol. 2025 Jan;231:116641. doi: 10.1016/j.bcp.2024.116641. PMID: 39742688. 10: Cao Y, Zheng M, Shi J, Si J, Huang G, Ji Y, Hou Y, Ge Z. X-ray-Triggered Activation of Polyprodrugs for Synergistic Radiochemotherapy. Biomacromolecules. 2025 Jan 13;26(1):579-590. doi: 10.1021/acs.biomac.4c01373. Epub 2024 Dec 27. PMID: 39727263. 11: Lin TH, Lin HY, Tseng PC. Enhancing anti-vascular endothelial growth factor with photodynamic therapy for polypoidal choroidal vasculopathy: A meta- analysis. Surv Ophthalmol. 2024 Dec 19:S0039-6257(24)00157-7. doi: 10.1016/j.survophthal.2024.12.006. Epub ahead of print. PMID: 39709034. 12: Tang S, Wen C, Shen T, Zhu B, Wang X, Wang Z, Fu L, Wen Y, Han M, Kuang X, Ma W, Shen H, Yan J. The involvement of YAP-TGFβ-SMAD-mediated fibrosis in primary inferior oblique overaction. Biochim Biophys Acta Mol Basis Dis. 2024 Dec 9;1871(3):167620. doi: 10.1016/j.bbadis.2024.167620. Epub ahead of print. PMID: 39662755. 13: Gao W, Song Y, Wu F, Xu S, Liu B, Zeng L, Zheng E, Song H, Zhang Q. Tumor- Targeted Metal-Organic Framework for Improved Photodynamic Therapy and Inhibited Tumor Metastasis in Melanoma. ACS Appl Mater Interfaces. 2024 Dec 18;16(50):69769-69788. doi: 10.1021/acsami.4c18058. Epub 2024 Dec 9. PMID: 39652639. 14: Yang TT, Liu Y, Shao YT, Li L, Pan DD, Wang T, Jiang ZZ, Li BJ, Qian ST, Yan M, Zhu X, Heng C, Liu JJ, Lu Q, Yin XX. Activation of MST1 protects filtration barrier integrity of diabetic kidney disease in mice through restoring the tight junctions of glomerular endothelial cells. Acta Pharmacol Sin. 2024 Dec 6. doi: 10.1038/s41401-024-01421-6. Epub ahead of print. PMID: 39643641. 15: Turcheniuk K, Turcheniuk V, Hage CH, Dumych T, Bilyy R, Bouckaert J, Héliot L, Zaitsev V, Boukherroub R, Szunerits S. Expression of concern: Highly effective photodynamic inactivation of E. coli using gold nanorods/SiO2 core-shell nanostructures with embedded verteporfin. Chem Commun (Camb). 2024 Dec 19;61(2):375. doi: 10.1039/d4cc90401j. PMID: 39635837. 16: Hu L, Zhang N, Zhao C, Pan J. Engineering ADSCs by manipulating YAP for lymphedema treatment in a mouse tail model. Exp Biol Med (Maywood). 2024 Nov 20;249:10295. doi: 10.3389/ebm.2024.10295. PMID: 39633684; PMCID: PMC11614642. 17: Yan S, Yang W, You W, He W, Yan J, Yao Y. Resurrecting p53 by an Artificial Nano-Protein for Potent Photodynamic Retinoblastoma Therapy. Small. 2024 Nov 30:e2401260. doi: 10.1002/smll.202401260. Epub ahead of print. PMID: 39614742. 18: Zhang P, Xu C, Liu Z, Geng Y, Liu H. Unleashing the therapeutic power of verteporfin-eluting stents: modulating YAP signaling to combat carotid artery restenosis and cerebral watershed infarction. Mol Cell Biochem. 2024 Nov 22. doi: 10.1007/s11010-024-05160-4. Epub ahead of print. PMID: 39576466. 19: Zhang X, Liu H, Wan C, Li Y, Ren C, Lu J, Liu Y, Yang Y. Verteporfin combined with ROCK inhibitor promotes the restoration of corneal endothelial cell dysfunction in rats. Biochem Pharmacol. 2025 Jan;231:116641. doi: 10.1016/j.bcp.2024.116641. Epub 2024 Nov 19. Erratum in: Biochem Pharmacol. 2024 Dec 31;232:116737. doi: 10.1016/j.bcp.2024.116737. PMID: 39571917. 20: Bloom J, Madani R, Haidar AJ, Alasil T. Faricimab Treatment of Polypoidal Choroidal Vasculopathy Resistant to Intravitreal Ranibizumab Injections and Ranibizumab Port Delivery (Susvimo). J Vitreoretin Dis. 2024 Aug 22:24741264241271739. doi: 10.1177/24741264241271739. Epub ahead of print. PMID: 39554622; PMCID: PMC11562463.
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