On November 10, 2022 Regen BioPharma, Inc. (OTC PINK: RGBP) and (OTC PINK: RGBPP) reported that it has recently discussed the use of CAR-T therapies in cancer treatment (View Source;explores-the-car-t-therapeutic-space-301660078.html) and its development of a novel approach to creating CAR-T cells that can potentially be used to treat solid tumors (View Source;develops-novel-dedifferentiation-approach-for-increasing-efficacy-of-car-t-cells-to-treat-solid-tumors-301604599.html).
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The tumor microenvironment contains molecules and cells which can suppress T cells and prevent them from attacking and killing the tumor. "T cell exhaustion" is a term that describes T cells that are initially recruited to a tumor to kill it but end up rapidly losing their effectiveness. Eventually the tumor is surrounded by T cells that are exhausted and ineffective.
The Company has focused on NR2F6, an immune checkpoint which has been convincingly shown to be a very important transcription factor that keeps T cells in check1-4. When this transcription factor is blocked, T cells become very active and can kill tumors much more effectively. The Company has coupled its proprietary shRNA technology, which inhibits NR2F6, with existing CAR-T cell technology to create a potentially durable CAR-T cell which cannot be exhausted by the solid tumor microenvironment. The Company calls this novel CAR-T cell DuraCAR.
"We believe DuraCAR has the characteristics to overcome several of the major hurdles in getting CAR-T cells to be effective in treating solid tumors," says Dr. David Koos Chairman and CEO of the company. "We will know more in the coming months from our experimental work how long the road will be to get our technology fine-tuned to the point where we have a proof-of-concept drug. It is very exciting to see our shRNA technology applied in a way that can potentially help so many people with cancer."
1Klepsch et al. Targeting the orphan nuclear receptor NR2F6 in T cells primes tumors for immune checkpoint therapy Cell Communication and Signaling (2020) 18:8. View Source
2Klepsch, V., Hermann-Kleiter, N., Do-Dinh, P. et al. Nuclear receptor NR2F6 inhibition potentiates responses to PD-L1/PD-1 cancer immune checkpoint blockade. Nature Communications (2018) 9, 1538. View Source
3Klepsch et. al. Beyond CTLA-4 and PD-1: Orphan nuclear receptor NR2F6 as T cell signaling switch and emerging target in cancer immunotherapy. Immunology Letters (2016) 178, 31-36. View Source
4Hermann-Kleiter, et. al. The Nuclear Orphan Receptor NR2F6 Is a Central Checkpoint for Cancer Immune Surveillance. Cell Reports (2015) 12:12, 2072-2085. View Source