Research

Kinevant Research

Mechanism

Cytokines

Cytokines

Cytokines are small proteins secreted by cells to regulate the body’s immune system. Cytokines act as molecular messengers capable of activating and attracting immune cells such as lymphocytes, neutrophils, and macrophages. Cytokines are key to understanding and manipulating the body’s immune response. Many cytokines such as IL-4, IL-6, and TNF-α are validated targets for treating inflammatory and autoimmune diseases.

Cytokines
Granulocyte macrophage colony stimulating factor (GM-CSF)

GM-CSF

Granulocyte macrophage colony stimulating factor (GM-CSF) is a pro-inflammatory cytokine that can activate macrophages and other immune cells to drive inflammation1,2. Multiple bodies of evidence demonstrate the potential key role that GM-CSF plays in the promotion and maintenance of sarcoid granuloma inflammation: GM-CSF is elevated in sarcoidosis patients and correlates with disease severity3, GM-CSF overexpression in animal models leads to granuloma formation, fibrosis, and tissue damage4, and animals without GM-CSF are unable to form granulomas despite being challenged by tuberculosis which would normally result in granuloma formation5.

Namilumab

Namilumab

Namilumab

Namilumab is an investigational, novel fully human monoclonal antibody conveniently administered once a month as a subcutaneous injection. Namilumab is a potent GM-CSF inhibitor that has been demonstrated well-tolerated in more than 300 patients so far across multiple clinical trials6. With Namilumab, our goal is to investigate the ability of namilumab to safely suppress the inflammation associated with sarcoidosis and significantly improve patients’ quality of life.

Namilumab

Clinical Trials

Kinevant has initiated a Phase 2 Clinical Trial investigating Namilumab in patients with chronic pulmonary sarcoidosis. For more information, please visit the RESOLVE-Lung study website.

 

Expanded Access Policy

Kinevant Clinical Trials

References

  1. Ishioka S, et al. Sarcoidosis, Vasculitis, and Diffuse Lung Diseases 1996.
  2. Itoh A, et al. Respirology 1998.
  3. Itoh A, Yamaguchi E, Furuya K, et al. Thorax 1993; Crouser ED, et al. Am J Respir Crit Care Med 2009; Itoh A, et al. Respirology 2008
  4. Xing Z, et al. J. Clin. Invest 1996.
  5. Szeliga J, Daniel DS, Yang CH, et al. Tuberculosis 2008; Beecher et al. Immunity 2016.
  6. Taylor P, et al. Arthritis Res Therapy 2019; Tanaka S et al. International J Pharmacol Therapy 2018; Papp KA et al. J Dermatol 2019; Huizinga TW et al. Arthritis Res Ther. 2017; Unpublished Ph 2 results ankylosing spondylitis