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Baricitinib and Alopecia Areata_MOD-MOA Video

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Baricitinib and Alopecia areata Chapter 1: Introduction & Unmet Needs in Alopecia Areata Alopecia areata, or AA, is an autoimmune hair loss disorder causing well-defined coin-shaped patches of non-scarring hair loss. Hair loss ranges from single well-defined patches, to multiple discrete or overlapping patches, to a loss of hair in all hair-bearing sites known as alopecia universalis. Alopecia areata affects nearly 2 percent of the population. Common comorbid disorders associated with alopecia areata include atopic dermatitis, thyroid disease, allergic rhinitis and vitiligo. Alopecia areata is also associated with psychiatric comorbidities such as anxiety and depression, affecting patients’ quality of life. Alopecia areata has a complex aetiology with an unpredictable disease course making management difficult. Currently there are no FDA-approved therapies, and the responses to current treatment options are variable. Chapter 2: Mechanism of Disease of Alopecia Areata The human hair cycle has four distinct phases: Anagen is the growth phase, catagen is the transitional phase and telogen is the resting phase. Towards the end of telogen, the hair is shed in the exogen phase, and the follicle remains empty until the onset of the next anagen phase. In alopecia areata, the cyclical nature of hair growth is disrupted. Hair prematurely leave the anagen phase, transitions through catagen, telogen and exogen phases and enters the kenogen phase, where the hair follicle remains empty and does not reenter the growth phase. The pathogenesis of alopecia areata and the interference of the hair growth cycle are believed to be phenomena resulting from loss of hair follicle immune privilege. Immune privilege is a complex mechanism that suppresses inflammation and promotes immune tolerance in the hair follicle. It protects the follicle from auto-immune attack which may be triggered by immunogenic alloantigen generated during anagen and exposed as a result of the apoptosis and necrosis associated with cyclical hair growth. Loss of immune privilege allows immune cells to infiltrate the hair follicle leading to an inflammatory swarm around the anagen hair bulb. Chapter 3: The JAK-STAT Pathway in Alopecia Areata The JAK-STAT pathway is a proinflammatory signaling pathway utilized by cytokines in alopecia areata. Cytokines such as IFN-𝛾 and IL-15 are mediated by JAK kinases of the JAK-STAT pathway. The pathway is activated when ligand binding induces the dimerization of receptor subunits. Receptor-associated JAKs then bind ATP and become active. Subsequent activation of STAT transcription factors, which translocate to the nucleus, regulate the transcription of genes involved in the production of pro-inflammatory cytokines responsible for disease maintenance in alopecia areata. Chapter 4: Mechanism of Action of Baricitinib in Alopecia Areata Baricitinib is an immunomodulator and JAK inhibitor, which modulates intracellular signalling of many proinflammatory cytokines. Baricitinib binding results in the inhibition of JAK activation. However, complete inhibition of these pathways would not be well tolerated, and baricitinib’s efficacy is balanced by its transient binding and short half-life. Attenuating the proinflammatory mechanisms of alopecia areata and rebalancing the immune system by targeting the JAK-STAT pathway with JAK inhibitors may offer new possibilities for the treatment of alopecia areata.

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Posted by: gabriella61 on Dec 15, 2021

Baricitinib and Alopecia Areata_MOD-MOA Video

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