NCT07216001

Role of Omega-DEK in Childhood Apraxia of Speech

• Status: Not Yet Recruiting
• Phase: Phase 2
• Study type: Interventional
• Enrollment: 34 (estimated)
• Sponsor: Claudia R. Morris · Academic / Other
• Sex: All
• Age: 2 Years – 6 Years
• Healthy volunteers: Not accepted

Summary

This is a 20-week study for children between 3 and 6 years old with confirmed childhood apraxia of speech (CAS). The study includes a 12-week open-label pilot feasibility study of an investigational drug (Omega-DEK) plus L-carnitine (Carnitor®), which is followed by an 8-week randomized, placebo-controlled discontinuation period among the same study participants.

Detailed description

Verbal apraxia (VA) is a severe neurological motor planning speech disorder of unknown etiology. It is a devastating disorder that is insufficiently recognized by general pediatricians and often goes unaddressed and improperly treated during critical years of speech and language development. The high prevalence of this disorder excludes it as an "orphan" disease, although like autism, it may have met the definition over a decade ago. However, inadequate awareness of this condition among practitioners renders it a neglected disorder. Confusion around this condition is reflected by the vast number of terms used to define it, including Childhood Apraxia of Speech, Developmental Apraxia, Developmental Dyspraxia, Speech Apraxia, and Speech Dyspraxia to name a few. Approximately half of children with autism spectrum disorders (ASD) have some degree of apraxia, although not all apraxic children are autistic. There is currently no recognized cure for VA, and it is thought to be a life-long condition. Standard treatment is extremely costly and involves intensive and frequent 1:1 speech therapy with a speech pathologist knowledgeable in VA. Typical response to therapy tends to be slow, and some children do not learn how to talk, thereby requiring alternate means of communication. Children with this disorder find it very difficult to correctly pronounce sounds, syllables, and words, despite intense effort. Intelligibility is poor, and some children remain completely speechless and require the use of augmentative communication devices, sign language and/or a picture exchange communication system. Many children with VA present with a unique but homogeneous group of neurological symptoms that affect coordination, muscle tone and sensory issues in addition to expressive speech delay, suggesting a common underlying mechanism of disease. Vitamin E (vit E) deficiency causes a constellation of symptoms that overlap those of speech apraxia, limb dyspraxia, hypotonia and sensory integration dysfunction (including abnormalities in proprioception, vestibular sensation, and pain interpretation) that often occur in VA and ASD. Low bioavailability of vit E will create an environment within the cell membrane where vital polyunsaturated fatty acids (PUFAs) are vulnerable to lipid peroxidation and early destruction. This can lead to a functional PUFA deficiency and neurological sequelae that may be reversible through supplementation with PUFA/vit E. In addition, PUFA supplementation increases utilization of vit E in the body. These two supplements may have synergistic effects at higher doses. An unexpected number of apraxic children have a carnitine deficiency, high antigliadin antibodies and carry a gluten-sensitivity major histocompatibility complex (HLA), suggesting abnormal fatty acid metabolism, increased oxidative stress and a potential link to gastrointestinal inflammation and gluten-sensitivity that creates a distinctive nutritional requirement in these children that may benefit from an investigational drug specifically formulated to targets unique deficiencies that contribute to VA. The researchers speculate that patients with gluten sensitivity or those carrying a celiac HLA with autism/VA may not have classic celiac disease, but perhaps a broader diagnosis of gluten-sensitivity associated with malabsorption and neurobehavioral consequences of nutritional deficiencies that needs consideration. The less sensitive celiac biomarker, antigliadin immunoglobulin G (IgG), frequently found in both ASD and VA may represent a biomarker that identifies an intervention-responder group. A recent double-blind randomized, placebo-controlled trial in irritable bowel syndrome concluded that a non-celiac gluten intolerance my exist, a concept in need of exploration in both ASD and VA. In this study, children between 3 and 6 years old with confirmed childhood apraxia of speech (CAS) will take an investigational drug (Omega-DEK) plus L-carnitine (Carnitor®) for 12 weeks. This open-label period of the study is followed by an 8-week blinded trial where participants will be randomized to continue taking Omega-DEK or to take a placebo. Additionally, 10 participants will be enrolled in a cohort with expanded follow-up to examine the feasibility of conducting a 12-month open-label trial of Omega-DEK plus L-carnitine in participants aged ≥2 years who have a working diagnosis of CAS, intestinal lymphangiectasia, or fat malabsorption syndrome (in isolation or associated with other medical conditions such as cystic fibrosis, celiac disease, etc.).

Conditions

• Childhood Apraxia of Speech
• Verbal Apraxia
• Autism

Interventions

Type	Name	Description
DRUG	Omega-DEK	Participants take 2 capsules, twice daily (BID).
DRUG	L-carnitine	Participants take 250 mg L-carnitine administered as a 2.5 mL oral solution twice daily (BID).
DRUG	Placebo	A placebo of palm kernel oil to match Omega-DEK is provided. Participants take 2 capsules, twice daily (BID).

Timeline

• Start date: 2026-05-01
• Primary completion: 2027-12-01
• Completion: 2027-12-01
• First posted: 2025-10-14
• Last updated: 2026-02-27

Locations

2 sites across 1 country: United States

Regulatory

• FDA-regulated drug study