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Brexucabtagene autoleucel// TECARTUS

CAR-T ( Chimeric antigen receptor -T cell therapy)

MECHANISM OF ACTION

Tecartus is a CD19-directed genetically modified autologous T cell immunotherapy, binds to
CD19-expressing cancer cells and normal B cells. Studies demonstrated that following anti-CD19 CAR T cell engagement with CD19-expressing target cells, the CD28 and CD3-zeta co-stimulatory domains activate downstream signaling cascades that lead to T cell activation, proliferation, acquisition of effector functions, and secretion of inflammatory cytokines and chemokines. This sequence of events leads to killing of CD19-expressing cells.

Route of elimination: none known

MECHANISM OF KIDNEY INJURY

In the clinical trials no mention/ in package insert mention AKI in 6% patient in ZUMA-3. I would think is possible same mechanism with other CAR-T therapies, from CRS leading to hypoperfusion

CLINICAL KIDNEY SYNDROME

n/a

CARDIOVASCULAR ADVERSE EFFECTS

HTN/ Hypotension, arrythmia, edema, VTE , bradycardia , paliptations

LYTE ABNORMALITIES

Hypokalemia, Hypomagnesemia, Hypoalbuminemia, Hyponatremia, Hypophosphatemia

RISK FACTORS

MITIGATION STRATEGIES

if CRS - tocilizumab

SUGGESTIONS 

Tocilizumab if CRS

NOTES/COMMENTS

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PHARMACOKINETICS

Molecular Weight

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Volume of Distribution

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Plasma Protein Binding

Metabolism

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Bioavailability

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Half-life elimination

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Time to peak

Maximal expansion in peripheral blood is 15 days after infusion

Excretion

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Dialyzable?

Unknown

REF:

PATHOLOGY SLIDES:

ENTRY UPDATES:

Marco Bonilla

Chicago/USA

Sep 25, 2022

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