Inflammatory bowel disease and plaque psoriasis are complicated diseases; however, there may be an opportunity to target the TYK2, a member of the JAK family, in these conditions.3-5

TYK2 is responsible for transducing a signal to initiate a cascade that ultimately results in upregulated genes, such as those associated with the expression of several inflammatory molecules.6

PF-06826647 is a once-daily oral TYK2 inhibitor under investigation in subjects with either inflammatory bowel disease or moderate to severe plaque psoriasis.1,2

JAK PATHWAY

JAK inhibition may be a factor in a number of inflammatory diseases, including alopecia areata, atopic dermatitis, Crohn's disease, non-segmental vitiligo, plaque psoriasis, psoriatic arthritis, rheumatoid arthritis, systemic lupus erythematosus, and ulcerative colitis.4,5,7-15

Figure adapted from Paller AS et al. J Allergy Clin Immunol. 2017;140(3):633-643.

  • Chronic idiopathic inflammatory diseases of the skin and gut are characterized by a hyperactive immune milieu containing upregulated chemokines, proinflammatory cytokines, and infiltration of an assortment of innate and adaptive immune cells7,16-19
  • The Janus kinase-signal transducer and activator of transcription (JAK-STAT) is a signaling pathway by which a number of proinflammatory cytokines (eg, IL-4, IL-13) may transduce their pathophysiological functions and contribute to immune hyperactivity7,16
  • The binding of a cytokine to its receptor leads to JAK activation, which in turn phosphorylates STATs. STATs then dimerize and translocate to the nucleus, where they may direct expression of a number of genes affecting differentiation of immune cells and lead to upregulated cytokines7,16

Now enrolling in PLAQUE PSORIASIS

For adults with moderate to severe plaque psoriasis2

PF-06826647 is an investigational TYK2 inhibitor.1

The kinase activity of TYK2 may play a role in the pathophysiology of several autoimmune diseases.4,8-10

This is a phase 2, randomized, double-blind, placebo-controlled, multicenter study to evaluate the safety and efficacy of PF-06826647 in subjects with moderate to severe plaque psoriasis.2

Planned countries for recruitment include: United States.2

VIEW STUDY DESIGN2

VIEW ENDPOINTS

PRIMARY ENDPOINTS2

  • Change from baseline of subjects with a Psoriasis Area and Severity Index 90 (PASI 90) response at week 16
  • Number of subjects with adverse events at week 16 through follow-up at week 44
  • Number of subjects with a clinically significant change in vital signs through week 40
  • Number of subjects with clinically significant treatment-emergent electrocardiogram findingsa through week 40
  • Number of subjects with a change in laboratory tests results through week 40

KEY SELECTED SECONDARY ENDPOINTS2

  • Percentage of subjects with PASI 50, PASI 75, and PASI 100 response at week 16
  • Percentage of subjects with Physician Global Assessment (PGA) of psoriasis score of “clear” or “almost clear” at week 16
  • Percent change and absolute score of Peak Pruritis Numerical Rating Scale (NRS) score at week 16

aClinically significant electrocardiogram findings include corrected QT (QTc) >450 milliseconds, QTc >500 milliseconds, change in QTc between 30 and 60 milliseconds, and change in QTc greater than or equal to 60 milliseconds.

VIEW ELIGIBILITY CRITERIA

KEY SELECTED INCLUSION CRITERIA2

  • 18 to 75 years of age with a diagnosis of plaque psoriasis (psoriasis vulgaris) for at least 6 months
  • PASI score of 12 or greater AND PGA score of 3 (moderate) or 4 (severe)
  • Plaque-type psoriasis covering at least 10% of total BSA

KEY SELECTED EXCLUSION CRITERIA2

  • Non-plaque forms of psoriasis
  • Drug-induced psoriasis
  • Current active infection, including Mycobacterium tuberculosis (TB)
  • Any history of malignancies
  • Require treatment with prohibited concomitant medication(s)
  • Positive for hepatitis B or C viruses, or HIV

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