Verteporfin
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MedKoo CAT#: 203120

CAS#: 129497-78-5

Description: 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

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Verteporfin
CAS# 129497-78-5

Theoretical Analysis

MedKoo Cat#: 203120
Name: Verteporfin
CAS#: 129497-78-5
Chemical Formula: C41H42N4O8
Exact Mass: 718.30
Molecular Weight: 718.790
Elemental Analysis: C, 68.51; H, 5.89; N, 7.79; O, 17.81

Price and Availability

Size Price Availability Quantity
5mg USD 95 Ready to ship
10mg USD 150 Ready to ship
25mg USD 325 Ready to ship
50mg USD 550 Ready to ship
100mg USD 950 Ready to ship
200mg USD 1650 Ready to ship
500mg USD 3250 Ready to ship
1g USD 5850 Ready to ship
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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/

Solubility Data

Solvent Max Conc. mg/mL Max Conc. mM
Solubility
DMSO 70.0 97.38
DMF 20.0 27.82
Water 0.0 0.01

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.

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    1: Karim SP, Adelman RA. Profile of verteporfin and its potential for the treatment of central serous chorioretinopathy. Clin Ophthalmol. 2013;7:1867-75. doi: 10.2147/OPTH.S32177. Epub 2013 Sep 19. Review. PubMed PMID: 24092965; PubMed Central PMCID: PMC3788817.

2: Ziemssen F, Heimann H. Evaluation of verteporfin pharmakokinetics--redefining the need of photosensitizers in ophthalmology. Expert Opin Drug Metab Toxicol. 2012 Aug;8(8):1023-41. doi: 10.1517/17425255.2012.701617. Epub 2012 Jul 5. Review. PubMed PMID: 22762303.

3: Chan WM, Lim TH, Pece A, Silva R, Yoshimura N. Verteporfin PDT for non-standard indications--a review of current literature. Graefes Arch Clin Exp Ophthalmol. 2010 May;248(5):613-26. doi: 10.1007/s00417-010-1307-z. Epub 2010 Feb 17. Review. PubMed PMID: 20162298.

4: Shah GK, Sang DN, Hughes MS. Verteporfin combination regimens in the treatment of neovascular age-related macular degeneration. Retina. 2009 Feb;29(2):133-48. doi: 10.1097/IAE.0b013e3181960a28. Review. PubMed PMID: 19202423.

5: Cruess AF, Zlateva G, Pleil AM, Wirostko B. Photodynamic therapy with verteporfin in age-related macular degeneration: a systematic review of efficacy, safety, treatment modifications and pharmacoeconomic properties. Acta Ophthalmol. 2009 Mar;87(2):118-32. doi: 10.1111/j.1755-3768.2008.01218.x. Epub 2008 Jun 13. Review. PubMed PMID: 18577193.

6: Kaiser PK. Verteporfin photodynamic therapy and anti-angiogenic drugs: potential for combination therapy in exudative age-related macular degeneration. Curr Med Res Opin. 2007 Mar;23(3):477-87. Review. PubMed PMID: 17355729.

7: Augustin AJ, Schmidt-Erfurth U. Verteporfin therapy and triamcinolone acetonide: convergent modes of action for treatment of neovascular age-related macular degeneration. Eur J Ophthalmol. 2006 Nov-Dec;16(6):824-34. Review. PubMed PMID: 17191188.

8: Fenton C, Perry CM. Verteporfin: a review of its use in the management of subfoveal choroidal neovascularisation. Drugs Aging. 2006;23(5):421-45. Review. PubMed PMID: 16823995.

9: Schmidt-Erfurth U, Michels S, Augustin A. Perspectives on verteporfin therapy combined with intravitreal corticosteroids. Arch Ophthalmol. 2006 Apr;124(4):561-3. Review. PubMed PMID: 16606885.

10: Wickens J, Blinder KJ. A preliminary benefit-risk assessment of verteporfin in age-related macular degeneration. Drug Saf. 2006;29(3):189-99. Review. PubMed PMID: 16524319.

11: Kaiser PK. Verteporfin therapy in combination with triamcinolone: published studies investigating a potential synergistic effect. Curr Med Res Opin. 2005 May;21(5):705-13. Review. PubMed PMID: 15969870.

12: Verteporfin Roundtable Participants. Guidelines for using verteporfin (Visudyne) in photodynamic therapy for choroidal neovascularization due to age-related macular degeneration and other causes: update. Retina. 2005 Feb-Mar;25(2):119-34. Review. PubMed PMID: 15689800.

13: Arita J, Okuyama T. [Preclinical and clinical profile of verteporfin, a potent photodynamic therapy drug for CNV secondary to AMD]. Nihon Yakurigaku Zasshi. 2004 Dec;124(6):435-44. Review. Japanese. PubMed PMID: 15572848.

14: Huber G, Levy J. Development of verteporfin therapy: a collaboration between pharmaceutical companies, device manufacturers and clinical investigators. Semin Ophthalmol. 2001 Dec;16(4):213-7. Review. PubMed PMID: 15513443.

15: Sickenberg M. Verteporfin therapy for subfoveal choroidal neovascularization in age-related macular degeneration: from clinical trials to clinical practice. Semin Ophthalmol. 2001 Dec;16(4):207-12. Review. PubMed PMID: 15513442.

16: Michels S, Schmidt-Erfurth U. Photodynamic therapy with verteporfin: a new treatment in ophthalmology. Semin Ophthalmol. 2001 Dec;16(4):201-6. Review. PubMed PMID: 15513441.

17: Gaynes BI, Fiscella RG. Safety of verteporfin for treatment of subfoveal choroidal neovascular membranes associated with age-related macular degeneration. Expert Opin Drug Saf. 2004 Jul;3(4):345-61. Review. PubMed PMID: 15268651.

18: Keam SJ, Scott LJ, Curran MP. Spotlight on verteporfin in subfoveal choroidal neovascularisation. Drugs Aging. 2004;21(3):203-9. Review. PubMed PMID: 14979737.

19: Yang YC. Preserving vision with verteporfin photodynamic therapy. Hosp Med. 2004 Jan;65(1):39-43. Review. PubMed PMID: 14964795.

20: Meads C, Hyde C. Photodynamic therapy with verteporfin is effective, but how big is its effect? Results of a systematic review. Br J Ophthalmol. 2004 Feb;88(2):212-7. Review. PubMed PMID: 14736777; PubMed Central PMCID: PMC1772007.

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