DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for cleft palate-lateral synechia syndrome — screening already-approved drugs against its 4-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleCleft palate-lateral synechia syndrome maps to a 4-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 cleft palate-lateral synechia syndrome 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
transforming growth factor beta 3 (TGFB3) — TGFB3 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 diodrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 1TGJ · 2.0 Å · ligand 1,4-DIETHYLENE DIOXIDE (DIO). Experimental structure, not a prediction.
What the evidence adds up to
A 1995 case report notes that cleft palate and congenital lateral alveolar synechia syndrome is rare, with the patient described being only the fourth case of bilateral alveolar synechia with isolated cleft palate in the world literature and the second from the United States. Just over 50 cases involving intraoral synechiae had been reported at that time, and the authors state there are no documented cases of lateral interalveolar synechiae without cleft palate. A 2014 report of a 12-week-old female infant with cleft palate and lateral synechia causing inability to fully open the mouth describes release of the synechia without complications; the authors note that although some researchers believe the syndrome is inherited in an autosomal recessive pattern, their case indicated a new mutation may cause the condition. A 2016 case report describes a 4-year-old child brought for cleft palate repair who had intraoral synechiae but no history of breathing or feeding difficulty beyond what was attributed to the cleft palate.
A 2009 mouse study describes the csp1 N-ethyl-N-nitrosourea-induced model of non-syndromic cleft palate caused by an intronic Prdm16 splicing mutation. Prdm16 encodes a transcriptional cofactor that regulates TGFbeta signalling, and the cleft palate in these mice appears to result from micrognathia and failed palate shelf elevation due to physical obstruction by the tongue, resembling human Pierre Robin sequence-like cleft secondary palate. The authors suggest PRDM16 should be considered a candidate for mutation in human clefting disorders, especially non-syndromic cleft palate and Pierre Robin sequence-like cleft palate. A 2012 review of the genetic basis of cleft lip and palate states that the etiology of non-syndromic cleft lip and palate is still largely unknown, with mutations in candidate genes identified in only a small proportion of cases. Three genes—TBX22, PVRL1, and IRF6—are responsible for X-linked cleft palate, cleft lip/palate-ectodermal dysplasia syndrome, and Van der Woude and popliteal pterygium syndromes respectively, and are also implicated in non-syndromic forms.
A 2025 systematic review of intraoral synechiae or bands in cleft palate synthesises evidence from 66 articles (1971–2024) documenting 90 cases, plus a new case, and proposes a standardised seven-subtype classification (A1–E) to enhance diagnosis and treatment planning. The protocol follows PRISMA guidelines and aims to improve multidisciplinary care and guide future research in this rare congenital anomaly. No drug treatment is mentioned in any of these abstracts.
What is still missing is a clear genetic or environmental cause for the majority of cases, large-scale genetic studies in humans to confirm candidate genes like PRDM16, and any pharmacological intervention—no drug has been tested or proposed for this syndrome. The rarity of the condition limits sample sizes for trials, and no patient stratification beyond anatomical subtypes has been validated.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Human Molecular Genetics · 2009 · 152 citations · open access
Prdm16 is required for normal palatogenesis in mice
AbstractTranscriptional cofactors are essential to the regulation of transforming growth factor beta (TGFbeta) superfamily signaling and play critical and widespread roles during embryonic development, including craniofacial development. We describe the cleft secondary palate 1 (csp1) N-ethyl-N-nitrosourea-induced mouse model of non-syndromic cleft palate (NSCP) that is caused by an intronic Prdm16 splicing mutation. Prdm16 encodes a transcriptional cofactor that regulates TGFbeta signaling, and its expression pattern is consistent with a role in palate and craniofacial development. The cleft palate (CP) appears to be the result of micrognathia and failed palate shelf elevation due to physical obstruction by the tongue, resembling human Pierre Robin sequence (PRS)-like cleft secondary palate. PRDM16 should be considered a candidate for mutation in human clefting disorders, especially NSCP and PRS-like CP.
Journal of Oral and Maxillofacial Pathology · 2012 · 137 citations · open access
A comprehensive review of the genetic basis of cleft lip and palate
AbstractCleft lip and palate (CLP) are birth defects that affect the upper lip and the roof of the mouth. CLP has a multifactorial etiology, comprising both genetic and environmental factors. In this review we discuss the recent data on the etiology of cleft lip and palate. We conducted a search of the MEDLINE database (Entrez PubMed) from January 1986 to December 2010 using the key words: 'cleft lip,' 'cleft palate,' 'etiology,' and 'genetics.' The etiology of CLP seems complex, with genetics playing a major role. Several genes causing syndromic CLP have been discovered. Three of them-T-box transcription factor-22 (TBX22), poliovirus receptor-like-1 (PVRL1), and interferon regulatory factor-6 (IRF6)-are responsible for causing X-linked cleft palate, cleft lip/palate-ectodermal dysplasia syndrome, and Van der Woude and popliteal pterygium syndromes, respectively; they are also implicated in nonsyndromic CLP. The nature and functions of these genes vary widely, illustrating the high vulnerability within the craniofacial developmental pathways. The etiological complexity of nonsyndromic cleft lip and palate is also exemplified by the large number of candidate genes and loci. To conclude, although the etiology of nonsyndromic CLP is still largely unknown, mutations in candidate genes have been identified in a small proportion of cases. Determining the relative risk of CLP on the basis of genetic background and environmental influence (including smoking, alcohol use, and dietary factors) will be useful for genetic counseling and the development of future preventive measures.
Cleft Palate and Congenital Lateral Alveolar Synechia Syndrome: Case Presentation and Literature Review
AbstractCleft palate and congenital lateral alveolar synechia syndrome remains a rare occurrence. Our patient represents only the fourth case of bilateral alveolar synechia with isolated cleft palate in the world literature and, as such, is only the second patient from the United States. More commonly, additional anomalies are associated. Just more than 50 cases involving intraoral synechiae have been reported. This group of cases has implications on fetal facial growth and cleft palate development because there are no documented cases of lateral interalveolar synechiae without cleft palate. Earlier reports can be grouped as variants along the spectrum. Theories of etiology are discussed.
Egyptian Journal of Ear Nose Throat and Allied Sciences · 2014 · 5 citations · open access
Cleft palate lateral synechia syndrome: Inhereditary or not?
AbstractAbstract Cleft palate lateral synechia syndrome (CPLS) is a very rare syndrome characterized by a cleft palate, adhesions in the mouth roof, some parts of the tongue or the mouth floor. This is a report of a 12-week-old female infant presented for evaluation of cleft palate, with lateral synechia that caused the inability to fully open the mouth. Release of the synechia was performed without complications. Although some researchers believe CPLS is inherited in an autosomal recessive pattern, our case indicated that a new mutation may cause this situation. Further research is recommended to clearly determine its inheredited and phenotypic variablities.
Journal of Cleft Lip Palate and Craniofacial Anomalies · 2016 · 5 citations · open access
Intraoral synechiae with cleft palate in an older child: A case report and review of literature
AbstractOral synechiae also called intraoral bands or congenital alveolar synechiae are extremely rare. The patient is usually a neonate with difficulty in breathing and feeding. We report the case of a 4-year-old child brought to the hospital for cleft palate repair having no history of breathing or feeding difficulty other than what was attributed to the cleft palate.
Open Science Framework · 2025 · 0 citations · open access
Intraoral Synechiae or Bands in Cleft Palate : Systematic Review with Proposed Classification
AbstractThis project presents a systematic review and case report titled "Intraoral Synechiae or Bands in Cleft Palate: A Case Report and Systematic Review with Proposed Classification." It synthesizes evidence from 66 articles (1971–2024) documenting 90 cases, plus a new case, to explore the clinical features, management, and outcomes of intraoral synechiae associated with cleft palate. A standardized seven-subtype classification (A1–E) is proposed to enhance diagnosis and treatment planning. The protocol, registered on the Open Science Framework (OSF), follows PRISMA guidelines, aiming to improve multidisciplinary care and guide future research in this rare congenital anomaly.
The Cleft Palate-Craniofacial Journal · 2025 · 0 citations
Bilateral Palatal Synechiae With Cleft Palate: A Rare Entity
AbstractLateral synechiae syndrome is a rare congenital malformation characterized by cleft palate and lateral intraoral adhesions from the free borders of the palate to the floor of the mouth. Synechiae can be isolated or occur more frequently in association with other congenital anomalies such as cleft lip and/or palate. These synechiae can cause functional deficits, especially in the respiratory and feeding difficulties, as well as facial abnormalities at later stages. Surgical excision of the adhesions as soon as possible is the well-adapted protocol at most centers. We report a case of a 15-day-old male infant reported to the outpatient department for feeding difficulties with a cleft palate associated with bilateral lateral intraoral synechiae.
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.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
