Vitiligo
Vitiligo, a persistent autoimmune condition, manifests as depigmented patches on the skin due to the loss of melanocytes. Our organization is wholly committed to pioneering inventive drug and therapy solutions that effectively tackle the complex challenges presented by vitiligo.
Overview of Vitiligo
Vitiligo is an advancing dermatological disorder that impacts around 1% of the worldwide populace, without regard to age, gender, or ethnic background. This condition is characterized by the emergence of depigmented skin patches resulting from the destruction of melanocytes, the specialized cells responsible for melanin production. These patches can manifest on various body regions, including the face, hands, feet, and genital areas.
The autoimmune hypothesis suggests that vitiligo is primarily driven by an aberrant immune response. CD8+ T cells have been identified as key players in the destruction of melanocytes. These T cells infiltrate the perilesional skin and produce cytotoxic effects, leading to melanocyte apoptosis. This immune-mediated destruction of melanocytes is further supported by the presence of melanocyte-specific CD8+ T cells in both the peripheral blood and vitiligo lesions.
Fig.1 Vitiligo pathogenesis. (Bergqvist C., et al., 2020)
Therapy Discovery and Development for Vitiligo
Vitiligo drug and therapy development aim to halt or reverse the progression of the disease, restore pigmentation, and improve the quality of life. The following are innovative vitiligo therapeutics that are currently being studied:
| Therapeutic groups | Drug type | Drug type |
|---|---|---|
| Afamelanotide + nbUVB versus nbUVB alone | Mc1R agonist | Stimulation of melanocyte stem cells |
| Simvastatin versus placebo | HMG-CoA reductase antagonist | Reduction of IFN-γ production |
| Topical ruxolitinib cream (no placebo) | JAK1/2 inhibitor | Inhibition of cytokine signaling |
| Topical ruxolitinib cream versus placebo | JAK1/2 inhibitor | Inhibition of cytokine signaling |
| ATI-50002 topical solution versus placebo | JAK3 inhibitor | Inhibition of cytokine signaling |
| PF-06651600 versus placebo; experimental extension for PF-06651600 versus placebo versus PF-06700841 versus nbUVB | JAK1/TYK2 inhibitor and JAK3 inhibitor | Inhibition of cytokine signaling |
| Topical ruxolitinib cream versus placebo | JAK1/2 inhibitor | Inhibition of cytokine signaling |
| Cerdulatinib gel versus placebo | JAK1/3, SYK inhibitor | Inhibition of cytokine signaling |
Within our esteemed organization, we take great pride in providing an extensive range of offerings tailored to vitiligo diagnostics and therapy development. If you possess an interest in exploring the remarkable therapeutic development services we offer, we kindly invite you to follow the link provided below.
Small Molecule Drug
Probiotics Therapy
Therapeutic Antibody
Cell Therapy
Gene Therapy
Therapeutics Development
Our Services
With a deep understanding of vitiligo's pathogenesis and the latest scientific advancements, our therapy development services encompass the discovery and development of novel therapeutic agents. We conduct rigorous preclinical research to evaluate the safety, efficacy, and mechanism of action of potential drug candidates targeting vitiligo-specific pathways.
Spontaneous Vitiligo Model
The spontaneous vitiligo model we offer involves the expression of membrane-bound hen egg lysozyme (HEL) in melanocytes under the control of the TRP-2 promoter. These mice are crossed with 3A9 CD4+ TCR mice, resulting in depigmentation of the hair, mediated by Fas-Fas ligand-mediated melanocyte killing.
TCR Transgenic Model
The models we provide involves the breeding of mice expressing a specific human MHC I molecule (HLA-A*021) with mice lacking the expression of tyrosinase. T cell clones that recognize the tyrosinase epitope (Tyr369) are isolated, and their TCR genes are used to generate TCR transgenic mice.
Melanoma-associated Vitiligo Models
Our company provides services for the development of a melanoma-associated vitiligo model. This model involves injecting melanoma cells into hosts and subsequent adoptive transfer of activated CD8+ T cell clones specific to melanocyte antigens, resulting in tumor regression and hair depigmentation.
In Vitro Models
At our company, we are at the forefront of vitiligo in vitro model development. In the context of vitiligo, we offer cell-based model and organoid model development services, including primary cell culture and the development of skin organoids of melanocytes, keratinocytes, and immune cells.
Our preclinical research services adhere to the highest scientific standards and regulatory guidelines, ensuring the robustness and reliability of the data generated. Beyond the aforementioned repertoire of services and models, our expertise extends to crafting personalized solutions and designing disease models that impeccably align with your unique needs. If our comprehensive range of offerings has piqued your interest, we wholeheartedly encourage you to connect with us without any hesitation.
References
- Bergqvist Christina, and Khaled Ezzedine. "Vitiligo: a review." Dermatology 236.6 (2020): 571-592.
- Frisoli Michael L., Kingsley Essien, and John E. Harris. "Vitiligo: mechanisms of pathogenesis and treatment." Annual review of immunology 38 (2020): 621-648.