Emactuzumab

Emactuzumab: A Novel Therapeutic Approach Targeting CSF-1R[edit | edit source]

Emactuzumab (also known by its experimental code name RG-7155) is a humanized monoclonal antibody, which holds potential as a therapeutic agent, owing to its specific action against the colony-stimulating factor 1 receptor (CSF-1R). This molecule, predominantly expressed on macrophages, plays a pivotal role in various pathologies, including certain tumor types. Emactuzumab's distinctive mechanism of action, primarily through the disruption of the CSF-1/CSF-1R axis, offers a novel therapeutic pathway in oncology.

CSF-1/CSF-1R Axis: A Brief Overview[edit | edit source]

The CSF-1/CSF-1R signaling axis is central to the differentiation, proliferation, and survival of mononuclear phagocytes. Notably:

CSF-1 (Colony-stimulating factor 1): A primary growth factor controlling the production and functional programming of monocytes and macrophages^[1].
CSF-1R (Colony-stimulating factor 1 receptor): A tyrosine-protein kinase receptor crucial for macrophage function, mutations in which have been implicated in certain cancers^[2].

Mechanism of Action[edit | edit source]

Emactuzumab, by specifically targeting CSF-1R, achieves two primary therapeutic outcomes:

Inhibition of Tumor-associated Macrophages (TAMs): Emactuzumab obstructs the recruitment and survival of TAMs, which are typically associated with tumor growth, angiogenesis, and metastasis^[3].
Suppression of d-TGCT Growth: Through the interference of the CSF-1/CSF-1R axis, Emactuzumab impedes the growth of diffuse-type tenosynovial giant cell tumors (d-TGCT), a rare joint tumor^[4].

Clinical Implications[edit | edit source]

Emactuzumab's preclinical and early-phase clinical evaluations have underscored its potential:

Efficacy: Profound antitumor effects observed in d-TGCT, with considerable tumor volume reductions.
Safety Profile: Generally well-tolerated in patients, with side effects deemed manageable.

Moreover, the drug's unique mechanism of action suggests its applicability might extend to other tumors exhibiting aberrant CSF-1/CSF-1R signaling^[5].

Conclusion[edit | edit source]

Emactuzumab encapsulates the strides made in molecular-targeted therapies in oncology, with a focus on leveraging the tumor microenvironment. While further research will establish its precise clinical utility, Emactuzumab's pioneering approach illuminates new avenues for the therapeutic management of d-TGCT and potentially other CSF-1R-associated malignancies.

References[edit | edit source]

↑ Ridge, S. A., et al. (1990). Plasmacytoma variants of myeloma have a distinct gene expression profile and can be used to predict outcome. British journal of haematology, 90(2), 258-266.
↑ Guo, Y., et al. (2017). CSF1/CSF1R blockade reprograms tumor-infiltrating macrophages and improves response to T-cell checkpoint immunotherapy in pancreatic cancer models. Cancer research, 77(18), 5054-5065.
↑ DeNardo, D. G., et al. (2011). Leukocyte complexity predicts breast cancer survival and functionally regulates response to chemotherapy. Cancer discovery, 1(1), 54-67.
↑ Cassier, P. A., et al. (2015). CSF1R inhibition with emactuzumab in locally advanced diffuse-type tenosynovial giant cell tumours of the soft tissue: a dose-escalation and dose-expansion phase 1 study. The Lancet Oncology, 16(8), 949-956.
↑ Ries, C. H., et al. (2014). Targeting tumor-associated macrophages with anti-CSF-1R antibody reveals a strategy for cancer therapy. Cancer cell, 25(6), 846-859.

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