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Vitiligo

It has been shown that melanocyte ferroptosis plays a role in the pathogenesis of vitiligo. As an innovative research service provider, Protheragen has specialized in diseases associated with iron metabolism. We provide a complete spectrum of services for researchers and scientists across the globe, ranging from diagnostics, therapeutics, and disease modeling to preclinical research. We extend our full attention to the complex interplay between vitiligo and iron metabolism disorders, offering an integrated, specialized multi-stage drug development service.

Overview of Vitiligo

The absence of functioning melanocytes results in white spots on the skin, which is referred to as vitiligo. These spots can lead to depigmented areas from a few millimeters to several centimeters. More recent studies suggest that vitiligo is associated with abnormal metabolism of iron. Dysregulation of iron homeostasis can lead to increased oxidative stress, which is an important factor in the development of vitiligo. Noticeable alterations in vitiligo individuals concerning some markers of ferroptosis and metabolism of iron suggest that iron-dependent cell death is critical for the loss of melanocytes.

Vitiligo pathogenesis mechanism. Fig.1 The mechanism behind vitiligo development. (Giri, P., Desai, D., and Dwivedi, M., 2024)

Iron Metabolism Abnormalities in Vitiligo

In vitiligo lesions, the overactive ferroptosis-related gene RRM2 is known to trigger the NF-κB signaling pathway, which consequently increases the production of inflammation-associated factors, including CXCL10 and IL-1β, that in turn lead to the recruitment of CD8⁺ T cells to destroy melanocytes. This NF-κB activation also accelerates and perpetuates melanocyte cell death from the upregulation of LCN2.

Oxidative stress plays a major role in the genesis of vitiligo by accumulating ROS in cells, which harms DNA, lipids, and proteins, and damages melanocytes. Additionally, oxidative stress releases HMGB1, impairing melanin production and mitochondrial function. Most importantly, high oxidative stress triggers ferroptosis in melanocytes because of their high iron uptake.

Therapeutics Development for Vitiligo

Drug Name	Mechanism of Action	Targets	Research Phase
Tanshinone IIA	Promote the translocation of Nrf2 into the nucleus as well as activate the Nrf2 pathway while preventing ferroptosis in melanocytes stimulated with H₂O₂.	Nrf2	Preclinical
Baicalein	Assist in melanocyte protection against ferroptosis by GPX4 overexpression.	GPX4	Preclinical
Curcumin	Regulate Nrf2/HO-1 pathway to protect melanocytes and inhibit ferroptosis.	Nrf2/HO-1	Preclinical

Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a therapy plan recommendation. For guidance on therapy options, please visit a regular hospital.

Our Services

Drawing upon our knowledge of iron metabolism, we provide comprehensive services for the entire scope of vitiligo drug development, from the earliest stages of discovery to preclinical validation. We provide all-inclusive support from the development of diagnostics, therapeutics, and disease models. Additionally, our pharmacokinetics and drug safety evaluation service preclinically evaluates the absorption, distribution, metabolism, excretion, and toxicological risk of your therapeutic candidates, ensuring their safety and efficacy.

Therapeutic Development Services

Animal Model Development Services for Vitiligo

Recognizing that relevant and reliable animal models are essential in the context of drug development, we provide tailor-made vitiligo animal models that accurately recapitulate the important components of the disease's pathogenesis to support vitiligo research with reliable research platforms.

Genetically Engineered Model

These models provide insight into the genetic basis of the disease by changing an animal's genes to induce the symptoms of vitiligo.

AAD + FH transgenic model
TrpHEL mouse model
h3TA2 mouse model
Pmel-1 mouse model
And more

Immunization-induced Model

Immunization-induced models simulate this autoimmune destruction by actively provoking an immune response targeting melanocytes in an animal.

Recombinant vaccinia virus-induced model
CD4 T cell depletion model
And more

Chemical-induced Model

These models involve the administration of certain chemicals to an animal, which leads to the destruction of melanocytes.

Monobenzone-induced model
Hydrogen Peroxide-induced model
Hydroquinone-induced model
And more

Pharmacokinetics and Drug Safety Evaluation Services

Pharmacokinetic Research Services
Physiochemical Studies	Bioavailability Studies
In Vitro Metabolism Studies	Metabolite Profiling and Identification Studies
In Vitro Permeability and Transporter Studies	Mass Balance Studies
Drug Absorption Studies	Biliary Excretion Studies
Quantitative Tissue Distribution Studies
Drug Safety Evaluation Services
General Toxicology Evaluation	Phototoxicity Evaluation
Genetic Toxicology Evaluation	Tissue Cross-Reactivity Evaluation
Developmental and Reproductive Toxicity Evaluation	Immunogenicity and Immunotoxicity Evaluation
Safety Pharmacology Evaluation	Toxicokinetics Evaluation
Local Toxicity Evaluation

Through the collaboration with Protheragen, you acquire unrivaled knowledge and a complete range of services focusing on advancing vitiligo and developing novel therapies related to iron metabolism. Ready to accelerate your vitiligo drug research and therapeutic development? Reach out to us and discuss how our tailored services can facilitate your next innovative achievement.

References

Wang, Ke et al. "Unveiling ferroptosis: a new frontier in skin disease research." Frontiers in immunology 15 (2024): 1485523.
Giri, Prashant et al. "Animal models unraveling the complexity of vitiligo pathogenesis." Autoimmunity reviews 23.4 (2024): 103515.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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