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Targeted Cancer Therapies

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Related Experiment Video

Updated: Apr 17, 2026

Non-Viral Engineering of Primary Human T Cells via Homology-Mediated End-Joining Targeted Integration of Large DNA Templates

Non-Viral Engineering of Primary Human T Cells via Homology-Mediated End-Joining Targeted Integration of Large DNA Templates

Published on: May 9, 2025

Redirection of genetically engineered CAR-T cells using bifunctional small molecules.

Min Soo Kim¹, Jennifer S Y Ma, Hwayoung Yun

¹California Institute for Biomedical Research , 11119 North Torrey Pines Road, Suite 100, La Jolla, California 92037, United States.

Journal of the American Chemical Society

|February 19, 2015

Summary

A novel folate-FITC molecular switch enables precise control over chimeric antigen receptor (CAR)-T cell therapy. This system enhances safety by targeting folate receptor-overexpressing tumors and allowing dose-dependent regulation of CAR-T cell activity.

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Last Updated: Apr 17, 2026

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Published on: February 16, 2015

Area of Science:

Immunotherapy
Oncology
Molecular Engineering

Background:

Chimeric antigen receptor (CAR)-engineered T cells (CAR-Ts) show potent antitumor activity but face safety challenges due to uncontrolled activation and expansion.
Current CAR-T cell therapies lack precise mechanisms for regulating T cell activity and terminating responses, posing safety risks.

Purpose of the Study:

To develop a novel bifunctional molecular switch for redirecting and regulating CAR-T cell activity.
To enhance the safety and specificity of CAR-T cell immunotherapy by controlling T cell responses.

Main Methods:

Developed a bifunctional small molecule switch: folate conjugated to fluorescein isothiocyanate (folate-FITC).
Utilized FITC-specific CAR-T cells and folate receptor (FR)-overexpressing tumor cells.
Assessed CAR-T cell cytotoxicity, activation, and proliferation in response to the folate-FITC switch and target cells.

Main Results:

The folate-FITC switch successfully redirected FITC-specific CAR-T cells to target FR-overexpressing tumor cells.
The system demonstrated high cytotoxicity against FR-positive cells with no activity against FR-negative cells.
CAR-T cell activation and proliferation were strictly dependent on the presence of both folate-FITC and FR-positive cells, and were dose-titratable.

Conclusions:

The folate-FITC molecular switch provides a controllable and specific method for engaging CAR-T cells with target tumors.
This novel treatment paradigm offers a potential strategy to improve the safety profile of CAR-T cell immunotherapy by enabling precise regulation of T cell activity.