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Cevostamab

Other names: RG6160; RO7187797

Modality: anti-FcRH5/CD3 bispecific antibody

Disease State: Relapsed or Refractory Multiple Myeloma

Summary

Cevostamab is an investigational T-cell engaging bispecific antibody designed to target Fc receptor-homolog 5 (FcRH5) on myeloma cells and cluster of differentiation 3 (CD3) on T-cells. This dual targeting is designed to activate and redirect T-cells to attack FcRH5-expressing myeloma cells.^1,2

Clinical Trials

Cevostamab

NCT ID	Study Phase	Enrollment Status	Study Title
NCT07555938	Phase III	Recruiting	Cevostamab in Combination With Pomalidomide and Dexamethasone Versus Standard of Care in Participants With Previously Treated Multiple Myeloma	View details
NCT05927571	Phase I	Recruiting	A Study Evaluating the Safety, Pharmacokinetics, and Activity of the Combination of Cevostamab and Elranatamab in Participants With Relapsed or Refractory Multiple Myeloma (R/R MM)	View details
NCT05583617	Phase I / Phase II	Recruiting	A Study Evaluating the Safety and Efficacy of Multiple Treatments in Participants With Multiple Myeloma	View details
NCT04910568	Phase I	Recruiting	A Study Evaluating the Safety, Pharmacokinetics, and Activity of Cevostamab in Participants With Relapsed or Refractory Multiple Myeloma	View details
NCT05535244	Phase I / Phase II	Active, not recruiting	A Study Evaluating the Efficacy and Safety of Cevostamab in Prior B Cell Maturation Antigen (BCMA)-Exposed Participants With Relapsed/Refractory Multiple Myeloma	View details

Proposed Mechanism of Action

FcRH5 is a type I membrane protein that is ubiquitously expressed on multiple myeloma cells.¹ FcRH5 is a multiple myeloma (MM) antigen with expression independent of B cell maturation antigen (BCMA).³

Cevostamab is a novel, first-in-class, T-cell engaging bispecific antibody proposed to bind to FcRH5, a B-cell lineage marker on myeloma cells and to CD3 on T cells^.1,2

Cevostamab is proposed to target the membrane-proximal domain of FcRH5 on myeloma cells and CD3 on T cells to facilitate an immunological synapse formation resulting in T-cell activation and killing of myeloma cells.^1-3

Granzymes and perforin are released by the T-cell at the immunological synapse. Perforin facilitates the transport of granzymes into the myeloma cell which induces apoptosis in target myeloma cells resulting in T-cell dependent cancer cell death.^1,2,4-6

Cevostamab Mechanism of Action

Ho PJ, Quach H, Delimpasi S, et al. Subcutaneous cevostamab demonstrates manageable safety and clinically meaningful activity in Relapsed/Refractory multiple myeloma (RRMM): First results from the Phase Ib CAMMA 3 study. Blood. 2025;146(Supplement 1):700-700. doi:10.1182/blood-2025-700
Li J, Stagg NJ, Johnston J, et al. Membrane-Proximal Epitope Facilitates Efficient T Cell Synapse Formation by Anti-FcRH5/CD3 and Is a Requirement for Myeloma Cell Killing. Cancer Cell. 2017;31(3):383-395. doi:10.1016/j.ccell.2017.02.001.
Cohen A, Susanibar-Adaniya S, Garfall A, et al. Phase 2 study of cevostamab consolidation following BCMA CAR T cell therapy: preliminary safety, efficacy, and correlative data from the “STEM” (Sequential T Cell-Engagement for Myeloma) trial. Blood. 2025;146(Supplement 1):699-699. doi:10.1182/blood-2025-699.
Chowdhury D, Lieberman J. Death by a thousand cuts: granzyme pathways of programmed cell death. Annu Rev Immunol. 2008;26:389-420. doi:10.1146/annurev.immunol.26.021607.090404
Dieckmann NMG, Frazer GL, Asano Y, Stinchcombe JC, Griffiths GM. The cytotoxic T lymphocyte immune synapse at a glance. J Cell Sci. 2016;129(15):2881-2886. doi:10.1242/jcs.186205
Trapani JA. Granzymes: a family of lymphocyte granule serine proteases. Genome Biol. 2001;2(12):REVIEWS3014. doi:10.1186/gb-2001-2-12-reviews3014

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