2 new JAK inhibitors secure expanded reimb

for ankylosing spondylitis

Reimb for JAK inhibitors, Xeljanz and Rinvoq, are expanded to include use for active ankylosing spondylitis, starting on the 1st

Biologic drugs Cosentyx and Taltz to receive expanded reimbursements…. as 1st-line treatments for active ankylosing spondylitis

The treatment market for active ankylosing spondylitis, which had been previously dominated by Tumor Necrosis Factor-alpha (TNF-α) inhibitors such as Humira and Remicade, is transforming.

 

As of the 1st of this month, reimbursement has been applied and expanded to include major Janus Kinase (JAK) inhibitors and biologic agents for treating active ankylosing spondylitis; thereby, forecasting a likely surge in market competition.

 

According to the industry on the 16th, the two JAK inhibitors, Pfizer’s Xeljanz (tofacitinib) and AbbVie’s Rinvoq (upadacitinib), newly passed the reimbursement criteria for treating active ankylosing spondylitis.

 

Eli Lilly’s Taltz (ixekizumab) and Novartis’ Cosentyx (secukinumab) now receive expanded reimbursement criteria for primary treatment options active ankylosing spondylitis.

 

Active ankylosing spondylitis is an autoimmune disease that involves inflammation in the spine and, over time, can cause progressive spinal rigidity.

 

The inflammation in spine joints results in pain and loss of flexibility.

 

If left untreated, active ankylosing spondylitis can restrict movements because the bones in the spine fuse in a fixed position.

 

Until now, TNF-α inhibitors were used as the first-line treatment for active ankylosing spondylitis.

 

Due to the lack of treatment options for patients who developed resistance, anticipation is rising on the effect the newly reimbursement treatments will provide to the field.

 

Xeljanz and Rinvoq, first JAK inhibitors to add reimbursement standards for active ankylosing spondylitis. Patients with severe active ankylosing spondylitis who have stopped receiving treatment due to poor response to one or more types of TNF-α inhibitor or IL-17A inhibitor will be able to receive reimbursement for the JAK inhibitors Rinvoq and Xeljanz.

 

JAK inhibitors suppress JAK enzymes., which play a critical role in facilitating processes in the immune system; however, their overactivation can lead to several autoimmune diseases.

 

JAK inhibor Pfizer

Rinvoq and Xeljanz proved effective in patients who failed prior treatments in clinical trials as well.

 

In the Phase 3 SELECT-AXIS 2 clinical studies, which enrolled patients with ankylosing spondylitis who failed previous treatments with TNF-α inhibitor or IL-17A inhibitor, the ASAS40 (Assessment of Spondyloarthritis International Society response standard improvement of 40% or more) response rate for patients treated with Rinvoq was 45.0% at week 14.

 

This was significantly higher than that of the placebo group (18.0%).

 

In the Phase 3 S-I clinical trial, which enrolled patients with active ankylosing spondylitis who had an inadequate response to prior TNF-α inhibitor treatments, the ASAS40 response rate for patients treated with Xeljanz was 41%, as opposed to 13% in the placebo group.

 

Due to the current expansion of reimbursement, the patients with active ankylosing spondylitis will be able to receive reimbursement for Xeljanz and Rinvoq, the drugs previously used for eczema, rheumatoid arthritis, and ulcerative colitis.

 

Notably, two drugs offer an advantage over other treatment options due to their convenience in administration, as they are oral treatments.

 

Cosentyx and Taltz, which are biologic drugs, succeeded in expanding the reimbursement criteria as first-line treatments for active ankylosing spondylitis The reimbursement criteria are expanded for Novartis's Cosentyx and Eli Lilly's Taltz, biologics that inhibit IL-17A, to include first-line treatments for ankylosing spondylitis.

 

Previously, reimbursement criteria were limited to cases where there was an inadequate response to one or more TNF-α inhibitors, or when treatment was discontinued due to side effects or incompatibility.

 

Cosentyx and Taltz both function by selectively binding to the cytokine IL-17A, an inflammatory mediator, and inhibiting its interaction with respective receptor.

 

IL-17 inhibitor Novartis

Through expanded reimbursement, Cosentyx and Taltz can now be used under the same criteria as TNF-α inhibitors.

 

The reimbursement criteria for these treatments have been expanded for patients with severe active ankylosing spondylitis who had shown insufficient response or drug side-effects despite treatment with two or more types of non-steroidal anti-inflammatory drugs (NSAIDs) or biological Disease-Modifying Anti-Rheumatic Drugs (bDMARDs) for over three months.

 

In the four-year long-term MEASURE 1 study, Cosentyx has shown that in approximately 80% of active ankylosing spondylitis patients, there was no progression of spinal deformity (modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) changes less than 2) over four years.

 

Moreover, the MEASURE 2 study demonstrated the long-term effect of Cosentyx in improving key symptoms of active ankylosing spondylitis, including morning stiffness, spinal pain, fatigue, and nocturnal back pain up to 5 years.

 

The effectiveness of Taltz was demonstrated in COAST-V clinical studies in patients who are biologic disease-modifying antirheumatic drug (bDMARD)-naïve, and COAST-W Phase 3 studies in patients who previously had an inadequate response or were intolerant to tumor necrosis factor (TNF) inhibitors.

 

The COAST-V clinical trial result demonstrated that the ASAS40 response rate for patients treated with Taltz was 48% at week 16, a significantly higher response rate compared to the 18% in the placebo group.

 

In addition, the COAST-W clinical trial also demonstrated a higher ASAS40 response rate for Taltz compared to the place group (Taltz: 25.4%, Placebo: 12.5%).

 

Cosentyx and Taltz have shown consistent results not only in clinical trials but also in real-world data, confirming their effectiveness and safety in real medical settings.