NIH grant: Phase 2: Development of an endocannabinoid microparticle formulation for the topical treatment of cutaneous manifestations of lupus erythematosus (1R44AR087266-01A1)

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NIH grant 1R44AR087266-01A1: Phase 2: Development of an endocannabinoid microparticle formulation for the topical treatment of cutaneous manifestations of lupus erythematosus
Institute: {'code': 'AR', 'abbreviation': 'NIAMS', 'name': 'National Institute of Arthritis and Musculoskeletal and Skin Diseases', 'admin_org_id': '12500006', 'admin_funding_url': ''}. PI: Andrew R Draganski. Award: $1007121.
Start: 2026-09-25T00:00:00.
ABSTRACT
Approximately 500,000 people in the U.S. suffer from cutaneous lupus lesions (CLE), with a significant impact on quality of life.4 Yet, there is no cure, the treatment options are limited, and no new drug has been FDA-approved for over 50 years.84 As such, CLE represents a high unmet need for directed therapeutics.
Skin lesions are caused by a complex autoimmune response dependent on genetic and environmental factors.80
These lesions have common histological features such as interface dermatitis with interferon-regulated chemokine expression.19 Anandamide (AEA) is a primary endocannabinoid involved in (i) modulation of the
innate and the adaptive immune system, (ii) processing of sensory input such as pruritus and pain, and (iii) maintenance of skin barrier integrity.152•153 AEA's primary pathway for decreasing inflammation is through binding
to CB2 receptors, which are predominantly expressed by macrophages and lymphocytes in peripheral organs with immune function, including the skin.164
AEA faces a variety of delivery challenges, however, including instability, limited penetration into the stratum corneum, and rapid metabolism by fatty acid amide hydrolase (FAAH).134-135To overcome these challenges,
AEA was loaded into a novel silica-derived particle delivery system for topicals that has been demonstrated to enhance bioavailability of several APls. The resulting formulation (AEA-ZP) was shown to (i) enhance penetration of AEA into the stratum corneum, (ii) provide extended release of AEA in the skin, and (iii) significantly reduce the size and severity of lupus lesions in three murine lupus studies as compared to controls, including unencapsulated AEA.
This Phase 11 proposal is a follow-up to the successful Phase I studies in which AEA-ZP was shown to be effective in treating lesions in a programmed death homolog 1 knockout mouse model. Also, improvements were made to the AEA-ZP fabrication process such that increased wt.% loading of AEA was achieved, thus removing a dosing limitation in toxicology studies and clinical trials to come.
During this Phase II proposal, mechanism of action studies will be performed on human lupus tissue and PBMC, a near-GMP demonstration batch of AEA will be synthesized, a final formulation-incorporating the AEA-ZP-will be developed at near-GMP level, safety and toxicity studies will be conducted to support an eventual IND filing, and a pre-IND meeting will be held with the FDA.
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