Sweet's syndrome, or acute febrile neutrophilic dermatosis, is a rare and complex inflammatory syndrome with symptoms like fever, elevated neutrophil count, along with skin lesions that are painful and reddish in color. Protheragen offers an end-to-end preclinical drug and therapy development platform focusing on sweet's syndrome and aiming to expedite advances in your research.
Sweet's syndrome is marked by acute inflammation of skin and the tissue beneath it. Outbreaks are streamlined through sudden development of tender red plaques or nodules along with fever and increased neutrophils in blood. Certain tumors, infections, use of specific drugs, or even idiopathic can potentially trigger the syndrome. The hallmark feature are the lesions themselves which usually appear in a symmetrical and distributed pattern, but can also affect other regions such as joints, the eye, or internal organs. Very few reliable epidemiological studies exist however it is commonly accepted that it is underdiagnosed.
The pathogenesis of sweet syndrome is characterized by an inappropriate immune reaction that results in the selective accumulation and activation of neutrophils in the skin and other tissues. Although the exact cause is unknown, an imbalance in some cytokines, including granulocyte colony-stimulating factor (G-CSF), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) is thought to cause it. These cytokines are vital for neutrophil genesis and their maturation and migration. The severe inflammatory response gives rise to the striking skin lesions and other systemic symptoms. Genetic factors, together with some environmental triggers, are believed to explain the complicated immunological sequence events in sweet-syndrome.
Fig.1 Sweet syndrome histopathology. (Filosa and Filosa et al., 2018)| Category | Drug Name | Target / Intervention | Mechanistic Validation/Model Data | Development Stage |
| Immunomodulators | Colchicine | Neutrophil chemotaxis inhibition | Response rate 75% (steroids: 80%) | Approved |
| Baricitinib | JAK/STAT inhibition | Case reports: ulcer healing time decreased by 40% | Phase II | |
| Biologics | Infliximab | TNF-α neutralization | Complete response 65% in steroid-resistant cases | Phase III |
| Vilobelimab | C5a inhibition | Phase II: granuloma volume decreased by 60% | Phase II | |
| Novel Agents | Disulfiram | Gasdermin D inhibition | Inhibits NETosis in neutrophil cultures | Preclinical |
| Imsidolimab | IL-36R antagonism | 80% reduction in neutrophil infiltration in 3D models | Phase II |
Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.
Protheragen offers a complete range of services to progress therapeutic aims to treat Sweet's Syndrome. Our group of expert scientists, dermatologists, and immunologists utilize the latest and advanced technologies to ensure progress in your research efforts. We focus on therapeutic development, diagnostics development, as well as disease model development.
In Vivo Pharmacokinetics Services
Protheragen offers comprehensive preclinical research capabilities aimed at progress in sweet-syndrome therapeutics, from discovery to preclinical development. Our state-of-the-art facilities and experienced team conduct rigorous in vitro and in vivo studies to evaluate the safety and efficacy of potential therapeutics, ensuring that your drug candidates meet the highest standards.
Partner with us to accelerate your sweet-syndrome research and transform therapeutic innovations into effective solutions. If you are interested in our services, please contact us.
References
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