SUMMARY

• CARVYKTI (ciltacabtagene autoleucel [cilta-cel]) is a B-cell maturation antigen (BCMA)-directed, genetically modified, autologous T-cell immunotherapy, which involves reprogramming a patient’s own T cells with a transgene encoding a chimeric antigen receptor (CAR) that identifies and eliminates cells that express BCMA.¹
• CARVYKTI is prepared from the patient’s peripheral blood mononuclear cells; these are enriched for T cells and genetically modified ex vivo to express a CAR comprising an anti-BCMA targeting domain, which consists of 2 single-domain antibodies linked to
  4-1BB costimulatory domain and a cluster of differentiation (CD)3-zeta (ζ) signaling domain.¹

PRODUCT LABELING

Description

• CARVYKTI is a BCMA-directed, genetically modified, autologous T-cell immunotherapy.¹
• CARVYKTI is prepared from the patient’s peripheral blood mononuclear cells, which are obtained via a standard leukapheresis procedure. The mononuclear cells are enriched for T cells and genetically modified ex vivo by transduction with a replication-incompetent lentiviral vector to express a CAR comprising an anti-BCMA targeting domain, which consists of 2 single-domain antibodies linked to a 4-1BB costimulatory domain and a CD3-ζ signaling domain.¹

Clinical Pharmacology

Mechanism of Action

• CARVYKTI is a BCMA-directed, genetically modified, autologous T-cell immunotherapy, which involves reprogramming a patient’s own T cells with a transgene encoding a CAR that identifies and eliminates cells that express BCMA.¹
• The CARVYKTI CAR protein features 2 BCMA-targeting single-domain antibodies designed to confer high avidity against human BCMA, a 4-1BB costimulatory domain and a CD3-ζ signaling cytoplasmic domain.¹
• Upon binding to BCMAexpressing cells, the CAR promotes T-cell activation, expansion, and elimination of target cells.¹

Literature Search

A literature search of MEDLINE^®, Embase^®, BIOSIS Previews^®, and Derwent Drug File databases (and/or other resources, including internal/external databases) was conducted on
21 November 2024.