ArticlePloS one2012
A high throughput screen identifies Nefopam as targeting cell proliferation in β-catenin driven neoplastic and reactive fibroproliferative disorders.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04685577 (A Randomized, Placebo Controlled, Double-Blind, Single Dose Study To Evaluate The Safety And Tolerability Of Cream In Burn Patients With Induced Dermal Incisions), which is not on this map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Randomized, Placebo Controlled, Double-Blind, Single Dose Study To Evaluate The Safety And Tolerability Of Cream In Burn Patients With Induced Dermal Incisions
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Repurposing neurological drugs for brain cancer therapeutics: A systematic approach to identify charged molecules for affinity-based local drug delivery systems.International journal of pharmaceutics · 2025Pooled it
- Clinical, mechanistic, and therapeutic landscape of cutaneous fibrosis.Science translational medicine · 2024Review
- Exploring the potential mechanism of WuFuYin against hypertrophic scar using network pharmacology and molecular docking.World journal of clinical cases · 2024Article
- Signaling pathways and their potential therapeutic utility in esophageal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Pharmacologic targeting of β-catenin improves fracture healing in old mice.Scientific reports · 2019Article
- Activated Signaling Pathways and Targeted Therapies in Desmoid-Type Fibromatosis: A Literature Review.Frontiers in oncology · 2019Review
- Immune Regulation of Skin Wound Healing: Mechanisms and Novel Therapeutic Targets.Advances in wound care · 2018Review
- β-Elemene inhibits the proliferation of primary human airway granulation fibroblasts by down-regulating canonical Wnt/β-catenin pathway.Bioscience reports · 2018Article
- Effects of chondroitin sulfate proteoglycan 4 (NG2/CSPG4) on soft-tissue sarcoma growth depend on tumor developmental stage.The Journal of biological chemistry · 2018Article
- Time Heals all Wounds- but Scars Remain. Can Personalized Medicine Help?Frontiers in genetics · 2018Article
- Scar management in burn injuries using drug delivery and molecular signaling: Current treatments and future directions.Advanced drug delivery reviews · 2018Review
- Wnt/β-catenin pathway in tissue injury: roles in pathology and therapeutic opportunities for regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Fibroproliferative disorders include neoplastic and reactive processes (e.g. desmoid tumor and hypertrophic scars). They are characterized by activation of β-catenin signaling, and effective pharmacologic approaches are lacking. Here we undertook a high throughput screen using human desmoid tumor cell cultures to identify agents that would inhibit cell viability in tumor cells but not normal fibroblasts. Agents were then tested in additional cell cultures for an effect on cell proliferation, apoptosis, and β-catenin protein level. Ultimately they were tested in Apc1638N mice, which develop desmoid tumors, as well as in wild type mice subjected to full thickness skin wounds. The screen identified Neofopam, as an agent that inhibited cell numbers to 42% of baseline in cell cultures from β-catenin driven fibroproliferative disorders. Nefopam decreased cell proliferation and β-catenin protein level to 50% of baseline in these same cell cultures. The half maximal effective concentration in-vitro was 0.5 uM and there was a plateau in the effect after 48 hours of treatment. Nefopam caused a 45% decline in tumor number, 33% decline in tumor volume, and a 40% decline in scar size when tested in mice. There was also a 50% decline in β-catenin level in-vivo. Nefopam targets β-catenin protein level in mesenchymal cells in-vitro and in-vivo, and may be an effective therapy for neoplastic and reactive processes driven by β-catenin mediated signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.