Fig. 1 · Structure

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Verteporfin

Cat. No. A12658 CAS 129497-78-5

YAP inhibitor

Verteporfin is a small molecule that inhibits TEAD, YAP association and YAP-induced liver overgrowth. It is also a potent second-generation photosensitizing agent derived from porphyrin.

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Publications for Verteporfin

8 publications citing this product

  1. Mouad Edderkaoui, .et al. , Int J Biol Sci, 2025, Oct 24;21(15):6907-6925 PMID: 41281751
  2. Szonja Anna Kovács, .et al. , British Journal ofPharmacology, 2025, 05 May PMID: 40324810
  3. Shruti Vig, .et al. , Cancer Drug Resist, 2024, Sep 21:7:35 PMID: 39403604
  4. Yu Ren, .et al. , Eur J Med Res, 2024, May 30;29(1):303 PMID: 38812041
  5. Po-Ju Lee, .et al. , J Exp Clin Cancer Res, 2022, Aug 20;41(1):254 PMID: 35986369
  6. Ling-Yan Liu, .et al. , Int J Mol Med, 2020, Dec;46(6):2235-2250 PMID: 33125123
  7. Wang Y, .et al. , Toxicol Appl Pharmacol, 2019, 2019 Dec 5;387:114852 PMID: 31812773
  8. Abe T, .et al. , Toxicol Sci, 2018, Oct 1;165(2):408-419 PMID: 29893953

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Biological Activity

Bioactivity / Mechanism

Verteporfin-related YAP immunoblot changes require careful interpretation. A light/dark comparison in three cell lines found additional high-molecular-weight YAP and phospho-YAP species when samples were processed under ambient light, with TEF1/TEAD1 comparatively resistant. This provides a potential photochemical confounder; the study did not directly measure YAP–TEAD binding or transcriptional inhibition. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
VDA (Endothelial cells)

In Vitro Studies

Verteporfin at 2 and 5 μM reduced population expansion of A375, mel-624 and mel-537 melanoma cells over five days relative to DMSO. This cell-count endpoint does not establish a biochemical inhibition constant or pathway selectivity. [2]

Verteporfin limits melanoma cell population expansion

Cell-based study · Human melanoma A375, mel-624 and mel-537 cells [2]

At 2 and 5 μM, verteporfin limited cell population expansion relative to DMSO over the displayed five-day time course. Cell counts, rather than an enzymatic target assay, define this endpoint. Growth inhibition alone does not establish target selectivity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell population expansion versus DMSO at day 5cell counts / fold population change p<0.05 for control versus experimental groups at 5 days (Figure 2 caption); no exact fold-change values extracted from curves[2]

Literature-Reported Treatment Conditions

Treatment concentration
2 and 5 μM
Exposure duration
5 days in Figure 2A
Method
Daily image-based cell counting; fold change relative to starting population
Vehicle
DMSO
Reported limits
Methods describe growth experiments minimally in triplicate; Figure 2 caption says triplicate, with at least five fields per experiment. Error-bar definition and a complete light-protection workflow are not specified in the read main text.
Methods and source locations

Compound reported in the paper: Verteporfin; Compound label in the paper: VP

Reported verteporfin experiments; no equivalence to an A12658 lot, isolated stereoisomer or clinical formulation is established.

Figure 2A and caption; Results: Both Verteporfin treatment and direct RNA-interference...; Methods: Cell culture and growth curves; Verteporfin timecourse; Figure 4A-B/caption; Methods: Cell length and morphology

Cell population expansion versus DMSO at day 5: Image-based counting in at least five fields per experiment; triplicate experiments reported — Figure 2A and caption; Results: Both Verteporfin treatment and direct RNA-interference...; Methods: Cell culture and growth curves; Verteporfin timecourse

Ambient-light handling changes verteporfin immunoblot readouts

Cell-based study · MEL270 uveal melanoma, HEK293 embryonic kidney and MCF-7 breast cancer cells; matched post-treatment lysates [1]

Under matched drug-treatment conditions, processing verteporfin samples in ambient light produced additional high-molecular-weight immunoreactive species compared with near-dark handling. This affected p62, DIAP1, ROCK1, YAP and phospho-YAP, with TEF1/TEAD1 comparatively resistant. VP-free light-exposed controls were included. These mobility changes are a confounder for interpreting apparent YAP depletion; the study did not directly test YAP–TEAD binding, reporter activity or target-gene transcription.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
High-molecular-weight immunoblot bands and monomeric immunoreactivity under matched light/dark processingqualitative immunoblot pattern Additional HMW species in light-processed VP samples; less VP-associated cross-linking under near-dark processing; TEF1/TEAD1 comparatively resistant[1]

Literature-Reported Treatment Conditions

Treatment concentration
1.25 µg/mL (LD) and 7.5 µg/mL (HD)
Exposure duration
0 h (immediate removal) or 6 h
Method
Matched dark treatment followed by ambient-light processing versus near-darkness throughout; immunoblotting
Vehicle
DMSO
Reported limits
Two independent biological replicates reported for Western blots. No quantitative target-binding potency was measured. Near-dark handling used minimal indirect red-filtered light; it was not absolute darkness.
Methods and source locations

Compound reported in the paper: Verteporfin; Compound label in the paper: VP

Reported verteporfin experiments; no equivalence to an A12658 lot, isolated stereoisomer or clinical formulation is established.

Figures 1A-C and 6A-C, images and captions; Results: Ambient light during sample processing... and YAP and phospho-YAP...; Methods: Cell lines and reagents, VP treatment and light/dark conditions, protein extraction and Western blot analysis; Discussion limitations

High-molecular-weight immunoblot bands and monomeric immunoreactivity under matched light/dark processing: Separate target membranes with β-actin loading controls; two independent biological replicates reported — Figures 1A-C and 6A-C, images and captions; Results: Ambient light during sample processing... and YAP and phospho-YAP...; Methods: Cell lines and reagents, VP treatment and light/dark conditions, protein extraction and Western blot analysis; Discussion limitations

In Vivo Studies

In a syngeneic pancreatic cancer metastasis model, verteporfin (25 mg/kg intraperitoneally, twice weekly for six weeks) reduced liver lesion number, the number of involved organs and metastatic score relative to saline control. The authors reported reductions of 60%, 30% and 50%, respectively. These findings describe this model and regimen and do not establish a YAP-specific mechanism. [3]

Activity varied by model and regimen. In BrafCA; Tyr-CreERT2; Ptenf/f mice, verteporfin at 4 or 6 mg/kg intraperitoneally every other day did not significantly delay melanoma lesion appearance. The paper also reported no significant reduction in terminal tumor volume or YAP/TAZ staining. Terminal collection is inconsistently labeled day 42 in Methods and day 45 in Results/caption; no single terminal day or dose-specific terminal effect is assigned here. [2]

No significant melanoma suppression in a transgenic mouse model

Animal study · BrafCA; Tyr-CreERT2; Ptenf/f mice with induced cutaneous melanoma [2]

Verteporfin did not significantly delay pigmented-lesion appearance or reduce terminal tumor volume relative to DMSO in this model. Tumor YAP/TAZ staining also showed no significant reduction. These are regimen-specific negative results, not evidence that all verteporfin regimens or all YAP-directed interventions lack activity.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Time to pigmented-lesion appearance versus DMSOlesion-free curve Lesions appeared between 18 and 21 days; Mantel-Cox P = 0.3462; Gehan-Breslow-Wilcoxon P = 0.5597[2]
Terminal tumor volume versus DMSOnormalized tumor volume p=0.262; no significant difference[2]
Terminal YAP/TAZ fluorescence normalized to DAPInormalized fluorescence p=0.326; no significant difference[2]

Conditions shared by the study groups

Route
Intraperitoneal injection
Frequency
Every other day
Treatment course
Every other day from the first day of melanoma induction until terminal collection; Methods say day 42, Results/Figure 6 say day 45
Vehicle
DMSO control; equivalent amount used
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Verteporfin regimens versus DMSO
4 and 6 mg/kg
DMSO vehicle controlNo significant change in lesion initiation; terminal pooled verteporfin group showed no significant tumor-volume or YAP/TAZ-staining reduction.[2]
Verteporfin regimens versus DMSO
Model: BrafCA; Tyr-CreERT2; Ptenf/f mice with induced cutaneous melanoma
Reported limits: Dose-specific animal group sizes and allocation of the pooled verteporfin terminal-volume/staining data are not explicit in the read main text. Terminal collection day conflicts (42 versus 45) and remains unresolved.
Methods and source locations

Compound reported in the paper: Verteporfin; Compound label in the paper: VP

Reported verteporfin experiments; no equivalence to an A12658 lot, isolated stereoisomer or clinical formulation is established.

Figure 6A-E and caption; Figure 5 timeline; Results: Verteporfin treatment of a mouse model...; Methods: Mouse Verteporfin treatments, immunohistochemistry and densitometry

Time to pigmented-lesion appearance versus DMSO: Daily observation; dose-specific curves at 4 and 6 mg/kg — Figure 6A-E and caption; Figure 5 timeline; Results: Verteporfin treatment of a mouse model...; Methods: Mouse Verteporfin treatments, immunohistochemistry and densitometry

Terminal tumor volume versus DMSO: External caliper volume; normalized to average DMSO volume; Figure 6C pools a verteporfin-treated category; no curve-derived means adopted — Figure 6A-E and caption; Figure 5 timeline; Results: Verteporfin treatment of a mouse model...; Methods: Mouse Verteporfin treatments, immunohistochemistry and densitometry

Terminal YAP/TAZ fluorescence normalized to DAPI: ImageJ densitometry: Results/Figure 6 describe 3 samples, 10 images/sample; Methods describe three independent slides/group. These sampling statements are not treated as animal n. — Figure 6A-E and caption; Figure 5 timeline; Results: Verteporfin treatment of a mouse model...; Methods: Mouse Verteporfin treatments, immunohistochemistry and densitometry

Verteporfin regimens versus DMSO · Figure 6A-E and caption; Figure 5 timeline; Results: Verteporfin treatment of a mouse model...; Methods: Mouse Verteporfin treatments, immunohistochemistry and densitometry

Reduced metastatic burden in a pancreatic cancer mouse model

Animal study · Syngeneic B6.129J mice (2–3 months old, males and females) bearing UNKPC961-Luc pancreatic cancer cells in a splenic liver-metastasis model [3]

Verteporfin treatment was associated with fewer liver lesions, fewer involved abdominal organs and a lower metastatic score than saline control. The authors reported reductions of 60%, 30% and 50%, respectively. This single-drug study does not establish a YAP-specific mechanism.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Liver lesion number, number of affected organs, and abdominal metastatic score versus controlreported reductions 60% fewer liver metastatic lesions; 30% fewer organs with lesions; 50% lower metastatic score[3]

Conditions shared by the study groups

Route
Intraperitoneal injection
Frequency
Twice weekly
Treatment course
6 weeks
Vehicle
Saline control; drug formulation not specified
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Verteporfin versus saline
25 mg/kg
Saline-treated tumor-bearing miceAuthor-reported reductions: 60% in liver lesion number, 30% in number of affected organs and 50% in metastatic score.[3]
Verteporfin versus saline
Model: Syngeneic B6.129J mice (2–3 months old, males and females) bearing UNKPC961-Luc pancreatic cancer cells in a splenic liver-metastasis model
Reported limits: Animal Methods state N = 6 without an explicit per-group allocation statement at that location. Blinded lesion assessment is reported. Drug formulation and a light-protection workflow are not specified in the read main text.
Methods and source locations

Compound reported in the paper: Verteporfin; Compound label in the paper: VP

Reported verteporfin experiments; no equivalence to an A12658 lot, isolated stereoisomer or clinical formulation is established.

Figure 6A-D image/caption; Results: YAP regulates metastasis in PDAC metastatic models in mice; Material and Methods: Chemicals, Animals, Statistics

Liver lesion number, number of affected organs, and abdominal metastatic score versus control: Blinded quantification; metastatic score incorporates lesion number and size in eight abdominal organs. Percentages are author-reported Results values, not recalculated from graph heights. — Figure 6A-D image/caption; Results: YAP regulates metastasis in PDAC metastatic models in mice; Material and Methods: Chemicals, Animals, Statistics

Verteporfin versus saline · Figure 6A-D image/caption; Results: YAP regulates metastasis in PDAC metastatic models in mice; Material and Methods: Chemicals, Animals, Statistics

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 129497-78-5
Applications YAP inhibitor
Formula C41H42N4O8
Molecular Weight 718.79
Synonyms Visudyne; DB00460; CL 318,952; Benzoporphyrin D; Bpd-MA; AIDS350621; Benzoporphyrin derivative monoacid ring A.
SMILES
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

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 89 mg/mL (123.82 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Baroutis KG, Corrêa VSMC, Ntentakis D, et al. Ambient light drives verteporfin-induced protein cross-linking during standard laboratory sample processing. PloS one (2026). PMID: 42766575 DOI: 10.1371/journal.pone.0358654 Source material
  2. [2] Lui JW, Xiao S, Ogomori K, et al. The Efficiency of Verteporfin as a Therapeutic Option in Pre-Clinical Models of Melanoma. Journal of Cancer (2019). PMID: 30662519 DOI: 10.7150/jca.27472 Source material
  3. [3] Edderkaoui M, Elmadbouh OHM, Lim A, et al. HDAC4/MybL1/YAP novel signaling axis is required for pancreatic cancer metastasis to the liver. International journal of biological sciences (2025). PMID: 41281751 DOI: 10.7150/ijbs.102132 Source material

Publications

8 publications citing this product

  1. Mouad Edderkaoui, .et al. , Int J Biol Sci, 2025, Oct 24;21(15):6907-6925 PMID: 41281751
  2. Szonja Anna Kovács, .et al. , British Journal ofPharmacology, 2025, 05 May PMID: 40324810
  3. Shruti Vig, .et al. , Cancer Drug Resist, 2024, Sep 21:7:35 PMID: 39403604
  4. Yu Ren, .et al. , Eur J Med Res, 2024, May 30;29(1):303 PMID: 38812041
  5. Po-Ju Lee, .et al. , J Exp Clin Cancer Res, 2022, Aug 20;41(1):254 PMID: 35986369
  6. Ling-Yan Liu, .et al. , Int J Mol Med, 2020, Dec;46(6):2235-2250 PMID: 33125123
  7. Wang Y, .et al. , Toxicol Appl Pharmacol, 2019, 2019 Dec 5;387:114852 PMID: 31812773
  8. Abe T, .et al. , Toxicol Sci, 2018, Oct 1;165(2):408-419 PMID: 29893953

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