DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for cystoid macular edema — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCystoid macular edema maps to a 3-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for cystoid macular edema is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
PHD finger protein 3 (PHF3) — PHF3 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet apo structuredrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6IC9 · 1.748 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
Cystoid macular edema (CME) is a common cause of visual loss in uveitis and often occurs after cataract surgery. In a 1988 study of 20 symptomatic eyes with clinical CME following extracapsular cataract extraction and posterior chamber intraocular lens implantation, resolution of symptoms and apparent resolution of the edema were observed in 18 (90%) of cases. Clearing occurred within one year in 14 (78%) of those 18 eyes and within two years in 17 (94%). In all eyes where the edema resolved, visual acuity returned to 20/40 or better, suggesting a relatively favourable course for this particular post-surgical presentation.
Treatment options include topical nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and carbonic anhydrase inhibitors. A 2008 prospective open-label pilot study of 15 patients with chronic CME (≥2 months) who were known steroid responders found that topical nepafenac 0.1% four times daily for 6 weeks, tapered over 6 weeks, produced a mean significant improvement in visual acuity and retinal thickness at 4 and 12 weeks compared to baseline (P < 0.0001). A subgroup of 11 patients with pseudophakic CME also showed significant improvement. A 2015 retrospective case series of six patients reported that a topical cocktail of strong steroid (difluprednate), NSAID, and carbonic anhydrase inhibitor drops achieved resolution of cystic edema with visual acuity improvement.
A 2025 retrospective chart review of 518 patients compared various treatment regimens for postoperative or uveitic CME. The combination of difluprednate and bromfenac (n = 28) showed the shortest mean resolution time (1.45 months). Tukey’s HSD test indicated this combination significantly outperformed other medications, reducing resolution times by 5.40 months compared to ketorolac alone (P = 0.0011), 4.76 months compared to ketorolac and prednisolone acetate (P = 0.0001), 5.42 months compared to loteprednol and nepafenac (P < 0.0001), 5.40 months compared to dexamethasone and nepafenac (P < 0.0001), and 4.47 months compared to no treatment (P = 0.0240). The difluprednate and bromfenac group had no cases of CME recurrence.
Despite these findings, a 2010 systematic review noted that placebo-controlled, double-masked, randomised clinical trials are largely lacking for pseudophakic CME. A 2007 review of inflammatory CME stated that treatment with anti-inflammatory and anti-VEGF drugs usually has a beneficial but temporary effect, and that there are no clear guidelines for treating subclinical CME in uveitis. The effect of vitrectomy in inflammatory CME is not yet clear. What remains missing are large, randomised controlled trials that directly compare the most promising topical combinations against each other and against intravitreal injections, with standardised outcome measures and longer follow-up to assess recurrence. Patient stratification by aetiology (post-surgical vs uveitic vs vitreoretinal interface disorders) and by steroid responsiveness is also needed.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Retina · 2010 · 114 citations
PHARMACOLOGIC THERAPY OF PSEUDOPHAKIC CYSTOID MACULAR EDEMA
AbstractPURPOSE: To review the current management and pharmacologic treatment of pseudophakic cystoid macular edema. METHODS: Systematic review of currently accepted treatment modalities for pseudophakic cystoid macular edema. Main outcome measures include visual acuity and retinal thickness measurement by optical coherence tomography. RESULTS: Optical coherence tomography is used to diagnose and monitor response to therapy. New topical nonsteroidal antiinflammatory drugs have been approved by the Food and Drug Administration for ophthalmic use, and some show promise in the treatment of pseudophakic cystoid macular edema. Other areas of clinical research include the use of anti-vascular endothelial growth factor agents and the addition of intravitreal routes of administration (e.g., corticosteroids, nonsteroidal antiinflammatory drugs, and anti-vascular endothelial growth factor agents). Surgical therapeutic options include Nd:YAG laser for anterior vitreolysis and pars plana vitrectomy for chronic refractory cases. CONCLUSION: Surprisingly, few changes have occurred in recent years in the treatment of pseudophakic cystoid macular edema. Placebo-controlled, double-masked, randomized, clinical trials are largely lacking.
Current Opinion in Ophthalmology · 2007 · 100 citations
Inflammatory cystoid macular edema
AbstractPURPOSE OF REVIEW: The aim of this article is to update our current understanding and management of inflammatory cystoid macular edema. RECENT FINDINGS: Cystoid macular edema is a common cause of visual loss in uveitis, which occurs predominantly in older patients with chronic uveitis forms and might be heralded by subclinical changes on optic coherence tomography. Cystoid macular edema is emerging as a major cause of visual loss in HIV-infected patients with immune recovery uveitis. Elevated levels of proinflammatory cytokines and vascular endothelial growth factor were found in all types of cystoid macular edema. Treatment with anti-inflammatory and anti-vascular endothelial growth factor drugs is widely applied for all forms of cystoid macular edema and usually has a beneficial, but temporary effect. So far, there are no clear guidelines for the treatment of subclinical cystoid macular edema in uveitis. The effect of vitrectomy in inflammatory cystoid macular edema is not yet clear and might become more important in the future. Recent advances in management include intravitreal drug delivery systems of cystoid macular edema-modifying drugs. SUMMARY: This review summarizes current thoughts on inflammatory cystoid macular edema focusing on the new, clinically relevant findings. Upcoming data on aqueous constituents in cystoid macular edema and imaging with the new generation of optic coherence tomography offer the hope that a better treatment strategy will soon be established.
CYSTOID MACULAR EDEMA FOLLOWING EXTRACAPSULAR CATARACT EXTRACTION AND POSTERIOR CHAMBER INTRAOCULAR LENS IMPLANTATION
AbstractThe outcome of clinical cystoid macular edema (CME) was studied in 20 symptomatic eyes in which extracapsular cataract extraction and posterior chamber intraocular lens implantation had been performed. Resolution of symptoms and apparent resolution of the macular edema were observed in 18 (90%) of the 20 cases. Clearing occurred within one year in 14 (78%) of these 18 eyes and in 17 (94%) within two years. In all eyes in which macular edema resolved, visual acuity returned to 20/40 or better. This study suggests that clinical cystoid macular edema occurring in association with a posterior chamber intraocular lens has a relatively favorable course.
TOPICAL NEPAFENAC AS AN ALTERNATE TREATMENT FOR CYSTOID MACULAR EDEMA IN STEROID RESPONSIVE PATIENTS
AbstractIn Brief Purpose: To evaluate the use of nepafenac 0.1% in patients with cystoid macular edema who are known steroid responders. Methods: Patients (N = 15) with clinical and angiographic cystoid macular edema (≥2 months) and a history of increased intraocular pressure following administration of topical corticosteroids participated in this prospective, open-label, pilot study. All patients were treated with nepafenac 0.1% four times daily for 6 weeks and the dose was tapered off over the ensuing 6 weeks. The total treatment duration was 12 weeks. Visual acuity and retinal thickness were measured. Results: For the entire population, there was a mean significant improvement in visual acuity and retinal thickness at 4 weeks and 12 weeks posttreatment compared with baseline (P < 0.0001). A subgroup analysis revealed that patients with pseudophakic cystoid macular edema (n = 11) had a mean significant improvement in visual acuity and retinal thickness compared with baseline at 4 weeks and 12 weeks posttreatment (P < 0.0001). Although the improvement in the vitreoretinal interface disorders group was not statistically different from baseline (probably due to the outlier), three of the four patients with vitreoretinal interface disorders had improvement in visual acuity and retinal thickness. Nepafenac was well tolerated. Conclusion: Nepafenac may be an effective and safe therapy for treating chronic cystoid macular edema in patients who are steroid responders. Patients (N = 15) with clinical and angiographic pseudophakic cystoid macular edema or cystoid macular edema associated with vitreoretinal interface disorders and a history of increased intraocular pressure following topical corticosteroids participated in this prospective, open-label, pilot study. Nepafenac effectively and safely improved visual acuity and retinal thickness.
International Medical Case Reports Journal · 2015 · 18 citations · open access
Strong topical steroid, NSAID, and carbonic anhydrase inhibitor cocktail for treatment of cystoid macular edema
AbstractPURPOSE: To report the combination cocktail of strong steroid, non-steroidal anti-inflammatory drug (NSAID), and carbonic anhydrase inhibitor drops for treatment of cystoid macular edema. METHODS: This is a retrospective case series of patients with cystoid macular edema managed with a topical combination of strong steroid (difluprednate), NSAID, and carbonic anhydrase inhibitor drops. The patients were followed with optical coherence tomography and fluorescein angiography. RESULTS: In our six cases, resolution of the cystic edema with improvement in visual acuity was achieved with the use of a combination cocktail of drops. Leakage on fluorescein angiography and cystic edema on optical coherence tomography both responded to treatment with the topical cocktail of drops. CONCLUSION: A topical cocktail of strong steroid, NSAID, and carbonic anhydrase inhibitor drops are effective for managing cystoid macular edema. Further studies comparing this combination with more invasive treatments should be undertaken to determine the efficacy of this cocktail over other treatment options.
Developments in ophthalmology · 2010 · 14 citations
Diagnosis and Detection
AbstractPURPOSE: To evaluate features of macular edema assessed by optical coherence tomography (OCT)and other imaging tools such as infrared, blue retinography and autofluorescence, and fluorescein and indocyanine green angiography (ICGA) in different pathologic conditions. METHODS: The principal causes of macular edema were reviewed to evaluate its aspect in each pathology. Correlations between OCT and other imaging techniques were analyzed. RESULTS: Optical coherence tomography and other imaging tools allowed the authors to confirm the existence of different macular edema patterns for different pathologies and to describe their characteristics; in particular, some conditions, like idiopathic macular telangiectasias and age-related maculopathy, were found to present specific edema patterns. CONCLUSIONS: Simultaneous use of different imaging techniques allowed a better evaluation and follow-up of conditions causing cystoid macular edema.
Clinical ophthalmology · 2025 · 0 citations · open access
A Retrospective Data Analysis of Patients Treated with Difluprednate and Bromfenac for Cystoid Macular Edema After Uveitis or Cataract Surgery
AbstractPurpose: Cystoid macular edema (CME) is a condition which severely limits central vision, often occurring secondary to cataract surgery or uveitis. Although commonly treated with non-steroidal anti-inflammatory agents and a corticosteroid adjunct, an optimal medication regime has not yet been evaluated. Hence, we present a comprehensive analysis of the efficacy and relapse rate associated with various agents to treat CME, such as Bromfenac and Difluprednate. Patients and Methods: A retrospective chart review was conducted on patients aged 18 and above diagnosed with postoperative or uveitic CME via optical coherence tomography from January 1, 2016, to December 31, 2023. Among these eligible patients, we investigated those treated with non-steroidal anti-inflammatory drugs (NSAIDs) and/or corticosteroids. The primary outcome was the duration until complete resolution of CME. Secondary outcomes included improvement of CME and the likelihood of CME recurrence after treatment. Statistical analysis involved ANOVA and Tukey's HSD test to compare treatment efficacy. Results: A total of 518 patients were analyzed. Difluprednate and bromfenac (n = 28) demonstrated the shortest mean resolution time (1.45 months) compared to other combinations. The ANOVA test revealed significant differences among treatment groups (F-value: 6.455, P-value: <0.00001), and Tukey's HSD test showed that difluprednate and bromfenac significantly outperformed other medications in treating cystoid macular edema (CME) by reducing resolution times by 5.40 months compared to ketorolac alone (P = 0.0011), 4.76 months compared to ketorolac and prednisolone acetate (P = 0.0001), 5.42 months compared to loteprednol and nepafenac (P < 0.0001), 5.40 months compared to dexamethasone and nepafenac (P < 0.0001), and 4.47 months compared to no treatment (P = 0.0240). Difluprednate and bromfenac also had no cases of CME recurrence. Conclusion: Difluprednate and bromfenac proved to be the most effective treatment regimen for cystoid macular edema (CME), resolving the condition in the shortest amount of time and requiring less frequent dosing.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
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