treatment

Anti-CSF-1R Monoclonal Antibody

<img loading="lazy" decoding="async" class="aligncenter size-full wp-image-625" src="http://cms.syndax.com/wp-content/uploads/2023/11/Uckelmann_Revumenib_ASH2018-1-1.png" alt="" width="1826" height="1178" />
Source: Kitko et al. J Clin Oncol. 2022;41:1864-1875.
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The CSF-1/CSF-1R pathway is a key pathway in chronic GVHD that regulates monocyte proliferation and macrophage differentiation and activity.1 CSF-1R signaling is critical for development and function of alternatively polarized macrophages, which can exert profibrotic and inflammatory functions. In chronic GVHD, monocytes and macrophages can mediate inflammation and fibrosis, inducing tissue damage.2,3,4 By inhibiting CSF-1R signaling, macrophage- and monocyte-dependent pathways involved with both inflammation and fibrosis, hallmarks of chronic GVHD progression, can be suppressed.
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References:
<ol>
<li>Hume and Macdonald. Blood. 2012;119:1810-1820.</li>
<li>Alexander et al. J Clin Invest. 2014;124:4266-4280.</li>
<li>MacDonald et al. Blood. 2017;129:13-21.</li>
<li>Jardine et al. J Clin Invest. 2020;130:4574-4586.</li>
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Colony stimulating factor-1 receptor, or CSF-1R, is a cell surface protein thought to control the survival and function of monocytes and macrophages.
In pre-clinical models, inhibition of signaling through the colony stimulating factor-1 (CSF-1) receptor has been shown to reduce the number of disease-mediating macrophages along with their monocyte precursors, which has been shown to play a key role in the fibrotic disease process underlying diseases such as chronic graft-versus-host disease (GVHD) and idiopathic pulmonary fibrosis (IPF).

Close-up view of two spherical cells with a translucent outer membrane and a central nucleus, set against a soft pink background

Anti-CSF-1R Monoclonal Antibody

Anti-CSF-1R mAb