A novel sunscreen formulation, broad spectrum UV protection for cancer prevention featuring photoreactivation to repair existing sun damage

The National Cancer Institute awarded Framergy Inc. $400,000 on September 1, 2026, under the Cancer Cause and Prevention Research program (CFDA 93.393) to develop a novel sunscreen formulation featuring broad-spectrum UV protection and photoreactivation to repair existing sun damage.

Framergy, in collaboration with Johns Hopkins University, will develop a multi-benefit sunscreen additive that integrates targeted scavenging of harmful compounds with DNA repair via photolyase delivery. The technology centers on titanium metal-organic frameworks (Ti-MOFs) designed to block UV light, absorb cancer-triggering byproducts of inorganic and organic sunscreens, and immobilize photolyase to improve stability and effectiveness of DNA repair. This dual-action strategy combines prevention of UV-induced damage with active repair of DNA lesions in a single additive. Preliminary studies by Framergy have validated the feasibility of utilizing Ti-MOFs for skin cancer prevention, with testing demonstrating that Ti-MOFs reduced skin exposure to UV-A and UV-B compared to current inorganic oxide filters.

Performance occurs in College Station, Texas, with a period of performance from September 1, 2026, to May 31, 2027. Framergy is a Service-Disabled Veteran-Owned Small Business. The award is structured as a Project Grant, the SBIR Phase I assistance type under the Cancer Cause and Prevention Research program, which supports discovery and development of mechanisms for cancer prevention and preventive interventions, including cancer chemoprevention and interception.

Abstract

Framergy, INC., in collaboration with johns hopkins university (JHU), will develop a multi-benefit novel sunscreen additive that integrates targeted scavenging of harmful compounds with DNA repair via photolyase delivery. According to the skin cancer foundation (SCF), skin cancer is the most common cancer worldwide, affecting 1 in 5 americans by age 70. National cancer institute (NCI) notes that sunscreen use reduces exposure to cancercausing UV radiation and also helps prevent actinic keratoses, which are scaly skin lesions that can lead to squamous cell carcinoma. The development of next-generation sunscreens is hindered by the photogenotoxicity of commonly used UV-a blocking inorganic oxides (tio₂ and ZNO), which produce reactive oxygen species (ROS) under UV/visible light, transforming organic carriers into carcinogenic byproducts. Additionally, the use of DNA repair enzymes is limited due to poor stability when applied to the skin. Framergy's titanium metal-organic frameworks (TI-mofs) offer a promising solution by providing a sunscreen additive that can enhance UV protection, capture toxic byproducts, and provide a substrate suitable for photolyase immobilization. To address these limitations, the team will utilize mofs to (1) block UV light, (2) absorb cancer-triggering byproducts of inorganic and organic sunscreens, and (3) immobilize photolyase for improved stability and more effective DNA repair. This dual-action strategy combines prevention of UV-induced damage with active repair of DNA lesions in a single sunscreen additive. Preliminary studies performed by framergy have successfully validated the feasibility of utilizing TI-mofs for skin cancer prevention. Extensive testing demonstrated that TI-mofs reduced skin exposure to UV-a and UV-b when compared to current inorganic oxide filters. Preliminary in vivo studies conducted by JHU using a mouse model showed that TI-mofs reduced erythema, edema, DNA damage, immune cell infiltration, and inflammatory cytokines more effectively than leading inorganic additives. At typical sunscreen loadings, TI-mofs exhibited an increase of 288% in UV absorbance compared to tio₂ and 38% compared to ZNO when incorporated into sunscreen formulations. In this phase i project, framergy will evaluate the adsorption profiles of photolyase enzymes within framergy's UV filtering TI-mofs. JHU department of dermatology will then test the ability of this new formulation to reduce UV-induced skin inflammation, pigmentation, and DNA damage using a mouse model. The mouse model is necessary to evaluate the integrated effects of UV exposure, skin inflammation, DNA damage, and photolyasemediated DNA repair in intact skin, which cannot be adequately reproduced using in vitro models. Photorepair activity of MOF-photolyase biocomposites will be validated by testing the ability of the formulations to repair CPD photoproducts.