ArticleTranslational vision science & technology2019
SRD005825 Acts as a Pharmacologic Chaperone of Opsin and Promotes Survival of Photoreceptors in an Animal Model of Autosomal Dominant Retinitis Pigmentosa.
Article in Translational vision science & technology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Functional rescue and AI analysis of a human inactivating GPCR mutation using a small molecule.EMBO molecular medicine · 2026Article
- Therapeutic Potential of Partial Retinoid Agonists against Vertebrate Rhodopsin Misfolding Disorders.ACS omega · 2025Article
- Small-Molecule Ligands of Rhodopsin and Their Therapeutic Potential in Retina Degeneration.International journal of molecular sciences · 2025Review
- Advances and therapeutic opportunities in visual cycle modulation.Progress in retinal and eye research · 2025Review
- Mechanisms of Rhodopsin-Related Inherited Retinal Degeneration and Pharmacological Treatment Strategies.Cells · 2025Review
- Rhodopsin-associated retinal dystrophy: Disease mechanisms and therapeutic strategies.Frontiers in neuroscience · 2023Review
- Nonretinoid chaperones improve rhodopsin homeostasis in a mouse model of retinitis pigmentosa.JCI insight · 2022Article
- Gene Therapy of Dominant CRX-Leber Congenital Amaurosis using Patient Stem Cell-Derived Retinal Organoids.Stem cell reports · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMutations in
methodsA tetracycline-inducible cell line was used to produce human wild-type and T17M opsin. A cell-free assay was used to study the impact of SRD005825 on binding of 9-cis-retinal to wild-type opsin. A cell-based assay was used to measure the effect of SRD005825 on the generation of rhodopsin by spectroscopy and Western blot and the transport of rhodopsin to the cell membrane by confocal microscopy. Mice bearing T17M
resultsSRD005825 competed with 9-cis-retinal for binding to wild-type opsin but promoted the formation of rhodopsin in HEK293 cells and the trafficking of T17M rhodopsin to the plasma membrane of these cells. T17M transgenic mice exhibited rapid retinal degeneration, but thinning of the outer nuclear layer representative of photoreceptor cell bodies was delayed by treatment with SRD005825. Electroretinography a-wave and b-wave amplitudes were significantly improved by drug treatment.
conclusionsSRD005825 promoted the reconstitution of mutant rhodopsin and its membrane localization. Because it delayed retinal degeneration in the mouse model, it has potential as a therapeutic for autosomal dominant retinitis pigmentosa. TRANSLATIONAL RELEVANCE: SRD005825 may be useful as a treatment to delay retinal degeneration in retinitis pigmentosa patients with rhodopsin mutations causing misfolding of the protein.
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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.