Emerging trends in clinical research on Janus kinase inhibitors for atopic dermatitis treatment

Shih, Pei-Yun; Li, Chia-Jung; Yong, Su-Boon

doi:10.1016/j.intimp.2023.111029

Cited by 3 publications

(3 citation statements)

References 76 publications

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“…Then, we moved on to the evaluation of the efficacy of the selected compounds on dampening the pro-inflammatory JAK/STATs signaling, the most crucial pathway implicated in cytokines synthesis [ 36 ]. To this aim, we compared DE and KL with the anti-inflammatory drug tofacitinib (TOFA), a well-known Janus kinase 1/3 (JAK1/3) inhibitor [ 37 , 38 ]. NHKs were stimulated with TNF-α for 24 h in the presence or absence of DE, KL, or TOFA, and the amount of the secreted IL-6 and IL-8 was evaluated.…”

Section: Resultsmentioning

confidence: 99%

“…These kinases play a key role in the host immune response leading to the activation of pro-inflammatory transcription factors, such as NF-κB and AP-1, thus ensuing release of various cytokines, chemokines, and inflammatory mediators. To reduce side effects of long-term therapies with GCs, several studies have investigated the use of JAK inhibitors, such as tofacitinib, for the treatment of several skin inflammatory diseases, with drug approval cases for conditions such as psoriatic arthritis [ 37 , 38 , 47 , 48 ]. As for GCs, the use of tofacitinib seems to be linked to side effects such as acne exacerbation, and it is debated whether the therapy with the inhibitor is also associated with the risk of incident venous thromboembolism [ 49 , 50 , 51 ].…”

Section: Discussionmentioning

confidence: 99%

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Skin Anti-Inflammatory Potential with Reduced Side Effects of Novel Glucocorticoid Receptor Agonists

Flori,

Mosca,

Kovacs

et al. 2023

IJMS

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Glucocorticoids (GCs) are commonly used in the treatment of inflammatory skin diseases, although the balance between therapeutic benefits and side effects is still crucial in clinical practice. One of the major and well-known adverse effects of topical GCs is cutaneous atrophy, which seems to be related to the activation of the glucorticoid receptor (GR) genomic pathway. Dissociating anti-inflammatory activity from atrophogenicity represents an important goal to achieve, in order to avoid side effects on keratinocytes and fibroblasts, known target cells of GC action. To this end, we evaluated the biological activity and safety profile of two novel chemical compounds, DE.303 and KL.202, developed as non-transcriptionally acting GR ligands. In primary keratinocytes, both compounds demonstrated anti-inflammatory properties inhibiting NF-κB activity, downregulating inflammatory cytokine release and interfering with pivotal signaling pathways involved in the inflammatory process. Of note, these beneficial actions were not associated with GC-related atrophic effects: treatments of primary keratinocytes and fibroblasts with DE.303 and KL.202 did not induce, contrarily to dexamethasone—a known potent GC—alterations in extracellular matrix components and lipid synthesis, thus confirming their safety profile. These data provide the basis for evaluating these compounds as effective alternatives to the currently used GCs in managing inflammatory skin diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Skin Anti-Inflammatory Potential with Reduced Side Effects of Novel Glucocorticoid Receptor Agonists

Flori,

Mosca,

Kovacs

et al. 2023

IJMS

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“…Biological molecules, including dupilumab, tralokinumab, omalizumab, and nemolizumab, have demonstrated significant efficacy in regulating the JAK / STAT pathway and inhibiting JAK . This is particularly relevant as the JAK / STAT pathway encompasses interleukins such as IL-4 , IL-13 , and IL-31 [ 88 ].…”

Section: Emerging Therapies and Therapeuticsmentioning

confidence: 99%

Unraveling Atopic Dermatitis: Insights into Pathophysiology, Therapeutic Advances, and Future Perspectives

Pareek,

Kumari,

Pareek

et al. 2024

Cells

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Atopic dermatitis (AD) is an inflammatory skin condition that frequently develops before the onset of allergic rhinitis or asthma. More than 10% of children are affected by this serious skin condition, which is painful for the sufferers. Recent research has connected the environment, genetics, the skin barrier, drugs, psychological factors, and the immune system to the onset and severity of AD. The causes and consequences of AD and its cellular and molecular origins are reviewed in this paper. The exploration of interleukins and their influence on the immunological pathway in AD has been facilitated by using relevant biomarkers in clinical trials. This approach enables the identification of novel therapeutic modalities, fostering the potential for targeted translational research within the realm of personalized medicine. This review focuses on AD’s pathophysiology and the ever-changing therapeutic landscape. Beyond the plethora of biologic medications in various stages of approval or development, a range of non-biologic targeted therapies, specifically small molecules, have emerged. These include Janus kinase (JAK) inhibitors like Baricitinib, Upadacitinib, and Abrocitinib, thus expanding the spectrum of therapeutic options. This review also addresses the latest clinical efficacy data and elucidates the scientific rationale behind each targeted treatment for atopic dermatitis.

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Advancing inflammatory skin disease therapy: Sustained tofacitinib release via electrospun fiber dressings

Gürtler,

Maltschik,

M. Güler Yildiz

et al. 2024

European Journal of Pharmaceutics and Biopharmaceutics

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Emerging trends in clinical research on Janus kinase inhibitors for atopic dermatitis treatment

Cited by 3 publications

References 76 publications

Skin Anti-Inflammatory Potential with Reduced Side Effects of Novel Glucocorticoid Receptor Agonists

Skin Anti-Inflammatory Potential with Reduced Side Effects of Novel Glucocorticoid Receptor Agonists

Unraveling Atopic Dermatitis: Insights into Pathophysiology, Therapeutic Advances, and Future Perspectives

Advancing inflammatory skin disease therapy: Sustained tofacitinib release via electrospun fiber dressings

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