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2018-05-15 07:15 CEST
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Novartis ARROW trial to assess mechanistic superiority of direct IL-17A inhibition (Cosentyx®) over IL-23 inhibition (Tremfya®*)

  • ARROW study to assess the mechanistic superiority of direct IL-17A inhibition (Cosentyx) over IL-23 inhibition (Tremfya®*) in clearing of Stelara®*-resistant psoriatic plaques[1]

  • This is the 100th trial with Cosentyx in the last 10 years, adding to the wealth of data[2]. Cosentyx has been prescribed to more than 150,000 patients to date[3]

  • Cosentyx has a broad head-to-head study program that includes FIXTURE, CLEAR, CLARITY, SURPASS and EXCEED clinical superiority trials[4]-[8]

Basel, May 15, 2018 - Novartis announced today the plan to initiate ARROW, a head-to-head proof of concept study to assess the mechanistic superiority of the direct inhibition of IL-17A with Cosentyx® (secukinumab) over the inhibition of IL-23 with Tremfya®* (guselkumab) in patients with psoriatic plaques resistant to treatment with Stelara®*[1]. Study results are expected in 2019.

"We know there are different immune mechanisms driving the clinical manifestations of psoriasis, including the involvement of joints, scalp, nails, palms and soles psoriasis. Results from the ARROW trial could help us learn more about the differences between the direct targeting of IL-17A and IL-23 in psoriasis," said Kristian Reich, M.D., Ph.D., Georg-August-University Göttingen and Dermatologikum Hamburg, Germany. "It's great to see Novartis leading the science in psoriasis, psoriatic arthritis and ankylosing spondylitis."

"Treating all manifestations of psoriasis in the most effective way is crucial for patients and physicians. We are proud to be driving scientific activities to elucidate the biologic pathways in these diseases with the goal of transforming treatment options for patients," said Shreeram Aradhye, Chief Medical Officer and Global Head, Medical Affairs, Novartis Pharmaceuticals.

The ARROW study objective is to assess the mechanistic superiority of Cosentyx® over Tremfya®* in controlling clinical activity in psoriatic plaques resistant to treatment with Stelara®*[1]. IL-23 independent pathways of IL-17A release are potentially involved in inflammation of other persistent localizations, including joints, scalp, nails, palms and soles psoriasis[9]. Up to 90% of people with psoriasis may develop nail or palmoplantar psoriasis[10],[11]. Nail psoriasis is an important predictor of psoriatic arthritis (PsA) which affects up to 40% of patients with psoriasis[12].

Cosentyx is the first fully-human biologic that specifically inhibits interleukin-17A (IL-17A), a cornerstone cytokine involved in the inflammation and development of psoriasis, ankylosing spondylitis (AS), and psoriatic arthritis (PsA)[13]-[16]. IL-17A is produced by both IL-23 dependent and IL-23 independent pathways, by various cells from both the innate immune system (which can be triggered by mechanical stress) and the adaptive immune system[9]. By acting directly on IL-17A, Cosentyx inhibits this cornerstone cytokine irrespective of where the IL-17A comes from[13].

This study is now the 100th trial with Cosentyx in the last 10 years, adding to the wealth of data[2]. Cosentyx has a broad head-to-head study program that includes FIXTURE, CLEAR, CLARITY, SURPASS and EXCEED clinical superiority trials[1],[4]-[8]. To date, Cosentyx has been prescribed to more than 150,000 patients with psoriasis, PsA and AS worldwide[3].

About ARROW[1]
ARROW (CAIN457A2403) is a global multicenter open label randomized proof of concept Phase 2a study designed to assess the mechanistic superiority of secukinumab 300 mg over guselkumab 100 mg in achieving the clearing of psoriatic skin plaques resistant to treatment with ustekinumab after 16 weeks. 40 patients will be randomized 1:1 to secukinumab or guselkumab and treated for 16 weeks. The primary endpoint of the study is the percentage of patients achieving clear or almost clear status of the ustekinumab-resistant plaques as assessed through the Total Clinical Score (TCS =<2). The mechanistic exploratory endpoints of this study will explore the hypothesis that the direct targeting of IL-17A is able to overcome IL-23 independent mechanisms of resistance, providing a more complete approach to the control of alternative pathways of psoriasis inflammation.

Disclaimer
This press release contains forward-looking statements within the meaning of the United States Private Securities Litigation Reform Act of 1995. Forward-looking statements can generally be identified by words such as "potential," "can," "will," "plan," "expect," "anticipate," "look forward," "believe," "committed," "investigational," "pipeline," "launch," or similar terms, or by express or implied discussions regarding potential marketing approvals, new indications or labeling for the investigational or approved products described in this press release, or regarding potential future revenues from such products. You should not place undue reliance on these statements. Such forward-looking statements are based on our current beliefs and expectations regarding future events, and are subject to significant known and unknown risks and uncertainties. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those set forth in the forward-looking statements. There can be no guarantee that the investigational or approved products described in this press release will be submitted or approved for sale or for any additional indications or labeling in any market, or at any particular time. Nor can there be any guarantee that such products will be commercially successful in the future. In particular, our expectations regarding such products could be affected by, among other things, the uncertainties inherent in research and development, including clinical trial results and additional analysis of existing clinical data; regulatory actions or delays or government regulation generally; global trends toward health care cost containment, including government, payor and general public pricing and reimbursement pressures; our ability to obtain or maintain proprietary intellectual property protection; the particular prescribing preferences of physicians and patients; general political and economic conditions; safety, quality or manufacturing issues; potential or actual data security and data privacy breaches, or disruptions of our information technology systems, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

About Novartis
Novartis provides innovative healthcare solutions that address the evolving needs of patients and societies. Headquartered in Basel, Switzerland, Novartis offers a diversified portfolio to best meet these needs: innovative medicines, cost-saving generic and biosimilar pharmaceuticals and eye care. Novartis has leading positions globally in each of these areas. In 2017, the Group achieved net sales of USD 49.1 billion, while R&D throughout the Group amounted to approximately USD 9.0 billion. Novartis Group companies employ approximately 124,000 full-time-equivalent associates. Novartis products are sold in approximately 155 countries around the world. For more information, please visit http://www.novartis.com.

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* Tremfya® and Stelara® are registered trademarks of Janssen Biotech, Inc.

References
      [1]    Expected to be available on clinicaltrials.gov imminently.
      [2]    Clinicaltrials.gov. Active trials include all those that are listed as recruiting, active but not recruiting, enrolling by invitation and not yet recruiting and completed. This list excludes all trials listed as suspended, terminated and withdrawn.
      [3]    Novartis. Data on file.
      [4]    Langley RG et al. Secukinumab in Plaque Psoriasis - Results of Two Phase 3 Trials. N Engl J Med 2014;371:326-38.
      [5]    Blauvelt A et al. Secukinumab is superior to ustekinumab in clearing skin of subjects with moderate-to-severe plaque psoriasis up to 1 year: Results from the CLEAR study. J Am Acad Dermatol. 2017 Jan;76(1):60-69.
      [6]    Bagel J et al. Secukinumab is Superior to Ustekinumab in Clearing Skin of Patients with Moderate to Severe Plaque Psoriasis: CLARITY, a Randomized, Controlled, Phase 3b Trial. Presented as poster 98 at The Winter Clinical Dermatology Conference - Hawaii. January 13, 2018.
      [7]    Effect of Secukinumab on Radiographic Progression in Ankylosing Spondylitis as compared to GP2017 (Adalimumab Biosimilar) (SURPASS). Available at: https://www.clinicaltrials.gov/ct2/show/NCT03259074. Last accessed November 2017.
      [8]    Efficacy of Secukinumab Compared to Adalimumab in Patients With Psoriatic Arthritis (EXCEED 1). Available at: https://clinicaltrials.gov/ct2/show/NCT02745080. Last accessed November 2017.
      [9]    Schett G et al. Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol. 2017 Nov 21;13(12):731-741.
      [10]  Baran R. The burden of nail psoriasis: an introduction. Dermatol. 2010:221 Suppl 1:1-5.
      [11]  Kumar B et al. Palmoplantar lesions in psoriasis: a study of 3065 patients. Acta Dermatol Venereol. 2002;82:192-5.
      [12]  Mease PJ et al. Managing patients with psoriatic disease: the diagnosis and pharmacologic treatment of psoriatic arthritis in patients with psoriasis. Drugs 2014;74:423-41.
      [13]  Cosentyx Summary of Product Characteristics. Novartis Europharm Limited. Available at: http://www.ema.europa.eu/ema/index.jsp?curl=pages/medicines/human/medicines/003729/human_med_001832.jsp&mid=WC0b01ac058001d124. Accessed April 2018.
      [14]  Smith JA et al. Review: The Interleukin 23/Interleukin 17 Axis in Spondyloarthritis Pathogenesis: Th17 and Beyond. Arthritis Rheumatol. 2014;66:231-41.
      [15]  Nestle FO et al. Mechanisms of disease psoriasis. N Eng J Med. 2009;361:496-509.
      [16]  Girolomoni G et al. Psoriasis: rationale for targeting interleukin-17. Br J Dermatol. 2012;167:717-24.

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