Atopic Dermatitis Connect
  • Saved

Pharmacokinetics of Ruxolitinib in Patients with Atopic Dermatitis Treated With Ruxolitinib Cream: Data from Phase II and III Studies

Pharmacokinetics of Ruxolitinib in Patients with Atopic Dermatitis Treated With Ruxolitinib Cream: Data from Phase II and III Studies

Source : https://link.springer.com/article/10.1007/s40257-021-00610-x

Background Pathogenesis of atopic dermatitis (AD) involves the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. A cream formulation of ruxolitinib, a potent selective JAK1/JAK2 inhibitor, was developed...

  • Saved

made a Post

JAK Inhibitors in Atopic Dermatitis

Atopic dermatitis (AD), also known as atopic eczema, is a chronic, pruritic, relapsing inflammatory dermatological condition. The exact cause of the disease is unknown; however, certain factors such as epigenetic, genetic, immunological, and environmental interactions with overlapping skin barrier defects are indicated in its pathogenesis.



Oral Janus kinase (JAK) inhibitors have been approved for use in treating patients with rheumatoid arthritis and other inflammation & immunity disorders. Signaling proteins linked to cytokine receptors activate transcription factors, called signal transducer and activator of transcription (STAT) and modulate the expression of thousands of genes associated with inflammatory processes. JAK inhibition of type 2 cytokine signaling has recently shown pruritic benefit in clinical trials. JAK inhibition is not restricted to systemic administration but has also been developed as a topical treatment option.




  • Which clinical trial endpoints would be most impactful for you in assessing a drug’s efficacy for atopic dermatitis (ex. IGA, EASI, SCORAD, pruritus, QOL)?

  • In what patient subset or severity would you consider using a JAK inhibitor?

  • Would the availability of a topical JAK impact the prescribing trends for topical calcineurin inhibitors or crisaborole?



Reference: https://www.cell.com/action/showPdf?pii=S0092-8674%2817%2930931-5 




  • 5yr
    All the listed end points are useful. When I read studies, I tend to look first to EASI scores, but when it comes to treating the individual patient in Show More
  • 5yr
    All the listed end points are useful. When I read studies, I tend to look first to EASI scores, but when it comes to treating the individual patient in Show More

Show More Comments

  • Saved

made a Post

JAK Inhibitors in Atopic Dermatitis

Atopic dermatitis (AD), also known as atopic eczema, is a chronic, pruritic, relapsing inflammatory dermatological condition. The exact cause of the disease is unknown; however, certain factors such as epigenetic, genetic, immunological, and environmental interactions with overlapping skin barrier defects are indicated in its pathogenesis.

Oral Janus kinase (JAK) inhibitors have been approved for use in treating patients with rheumatoid arthritis and other inflammation & immunity disorders. Signaling proteins linked to cytokine receptors activate transcription factors, called signal transducer and activator of transcription (STAT) and modulate the expression of thousands of genes associated with inflammatory processes. JAK inhibition of type 2 cytokine signaling has recently shown pruritic benefit in clinical trials. JAK inhibition is not restricted to systemic administration but has also been developed as a topical treatment option.

  • Which clinical trial endpoints would be most impactful for you in assessing a drug’s efficacy for atopic dermatitis (ex. IGA, EASI, SCORAD, pruritus, QOL)?
  • In what patient subset or severity would you consider using a JAK inhibitor?
  • Would the availability of a topical JAK impact the prescribing trends for topical calcineurin inhibitors or crisaborole?

Reference: https://www.cell.com/action/showPdf?pii=S0092-8674%2817%2930931-5 

  • 5yr
    All the listed end points are useful. When I read studies, I tend to look first to EASI scores, but when it comes to treating the individual patient in Show More
  • 5yr
    All the listed end points are useful. When I read studies, I tend to look first to EASI scores, but when it comes to treating the individual patient in Show More

Show More Comments

  • Saved

made a Post

JAK Inhibitors in Atopic Dermatitis

Atopic dermatitis (AD), also known as atopic eczema, is a chronic, pruritic, relapsing inflammatory dermatological condition. The exact cause of the disease is unknown; however, certain factors such as epigenetic, genetic, immunological, and environmental interactions with overlapping skin barrier defects are indicated in its pathogenesis.



Oral Janus kinase (JAK) inhibitors have been approved for use in treating patients with rheumatoid arthritis and other inflammation & immunity disorders. Signaling proteins linked to cytokine receptors activate transcription factors, called signal transducer and activator of transcription (STAT) and modulate the expression of thousands of genes associated with inflammatory processes. JAK inhibition of type 2 cytokine signaling has recently shown pruritic benefit in clinical trials. JAK inhibition is not restricted to systemic administration but has also been developed as a topical treatment option.




  • Which clinical trial endpoints would be most impactful for you in assessing a drug’s efficacy for atopic dermatitis (ex. IGA, EASI, SCORAD, pruritus, QOL)?

  • In what patient subset or severity would you consider using a JAK inhibitor?

  • Would the availability of a topical JAK impact the prescribing trends for topical calcineurin inhibitors or crisaborole?



Reference: https://www.cell.com/action/showPdf?pii=S0092-8674%2817%2930931-5 




  • 5yr
    All the listed end points are useful. When I read studies, I tend to look first to EASI scores, but when it comes to treating the individual patient in Show More
  • 5yr
    All the listed end points are useful. When I read studies, I tend to look first to EASI scores, but when it comes to treating the individual patient in Show More

Show More Comments