Jiangsu Vcare Initiates Phase II Clinical Trial of VC005 Tablets, a Second-Generation Highly Selective JAK1 Inhibitor, for Oral Treatment of Vitiligo

　　Recently, Jiangsu Vcare PharmaTech Co., Ltd. (Jiangsu Vcare) officially initiated the Phase II clinical trial of VC005 Tablets, a second-generation highly selective JAK1 inhibitor independently developed by the company, for a new oral indication – the treatment of non-segmental vitiligo (NSV). This marks another new indication for VC005 Tablets following its application in the oral treatment of moderate-to-severe atopic dermatitis, ankylosing spondylitis, and rheumatoid arthritis. It signifies the further expansion of this product in the field of skin autoimmune disease treatment and is expected to bring a new treatment option to vitiligo patients.

　　This trial is a multicenter, randomized, double-blind, placebo-controlled Phase II clinical study designed to evaluate the efficacy and safety of VC005 in adult NSV patients in China. It also aims to assess the PK characteristics of VC005 Tablets in NSV patients, providing crucial evidence for subsequent clinical development.

　　In May 2025, after VC005 Tablets officially obtained IND approval from the NMPA, Jiangsu Vcare promptly advanced and launched this Phase II clinical study targeting NSV. Prior to this, VC005 oral tablets had demonstrated favorable efficacy and safety in clinical studies for the treatment of moderate-to-severe atopic dermatitis and ankylosing spondylitis, and both indications are currently in the Phase III clinical stage.

　　About VC005

　　VC005 Tablets is a novel, potent, and highly selective second-generation JAK1 inhibitor, for which Jiangsu Vcare holds independent intellectual property rights. In August 2025, Jiangsu Vcare entered into an exclusive strategic cooperation with Huadong Medicine regarding the commercialization rights of VC005 Tablets in Mainland China. By selectively inhibiting JAK1, VC005 Tablets reduces inflammatory responses and the activation of immune cells. Currently, the molecule has been developed for multiple autoimmune diseases such as moderate-to-severe atopic dermatitis, ankylosing spondylitis, rheumatoid arthritis, and vitiligo, with two dosage forms under development: oral tablets and topical gel. While maintaining strong JAK1 inhibitory activity, VC005 Tablets further reduces JAK2 inhibitory activity in a selective manner (based on in vitro kinase assay results), which is expected to alleviate safety issues caused by excessive JAK2 inhibition in clinical practice.

　　About Vitiligo

　　Vitiligo is an acquired depigmenting skin disorder. Currently, it is believed that the occurrence of depigmentation in the skin, mucous membranes, or hair is mainly caused by the specific destruction of local melanocytes by autoreactive T cells. The global incidence of vitiligo is approximately 0.5%-2%. Clinically, it is characterized by hypopigmented or depigmented macules, usually milky white in color, with clear boundaries, vary in sizes and shapes. Most patients have no subjective symptoms, and the disease is difficult to heal spontaneously. The pathological features of vitiligo include melanocyte death and CD8+ T cell infiltration, with CD8+ T cells preferentially localized in melanocytes at the lesional borders. The reversal of the disease can be achieved through immunosuppression and melanocyte regeneration. The function and continuous recruitment of CD8+ T cells are crucial for the progression of vitiligo. The cytokine IFN-γ produced by CD8+ T cells is the core cytokine triggering vitiligo, and autoreactive resident memory T cells (Trm cells) play a key role in the recurrence of vitiligo.

　　VC005 has a clear targeted mechanism of action. In vitiligo patients, on one hand, it inhibits the IFN-γ - JAK1/2 - STAT1 signaling pathway, blocking keratinocytes from releasing chemokines that recruit more CD8+ T cells; on the other hand, it inhibits the IL-15 - JAK1/3 - STAT3/5 signaling pathway, suppressing the activation of Trm cells. These actions are expected to achieve disease reversal and delay recurrence.