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Chimeric antigen receptors (CARs) are hybrid proteins consisting of an antibody binding fragment fused to protein signaling domains that cause T-cells which express the CAR to become cytotoxic.  Once activated, these cytotoxic T-cells can selectively eliminate the cells which they recognize via the antibody binding fragment of the CAR.  Thus, by engineering a T-cell to express a CAR that is specific for a certain cell surface protein, it is possible to selectively target those cells for destruction.  This promising new therapeutic approach is known as adoptive cell therapy.

Chimeric antigen receptors (CARs) combine an antibody-based binding domain (and single chain fragment variable region, scFv) with T cell receptor signaling domains (CD3 zeta with a costimulatory domain, typically CD28 or 41BB). When T cells express CARs, they are activated in a major histocompatibility complex- (MHC) independent manner to kill tumor cells expressing the target to which the scFv binds.  CAR T cells targeting the B cell antigen CD19 have resulted in remissions in 60-80% of patients with pre-B cell precursor acute lymphoblastic leukemia (BCP-ALL).

Adoptive T cell therapy (ACT) with tumor infiltrating lymphocytes (TIL), T cell receptor (TCR) and Chimeric Antigen Receptor (CAR) engineered T cells, or hematopoietic stem cell transplantation, is a promising new approach to cancer treatment. ACT harnesses an individual's adaptive immune system to fight against cancer, with fewer side-effects and more specific anti-tumor activity. Despite their promise of ACT as curative, these therapies are often limited by the persistence and robustness of the responses of the T cells to the cancer cells.

The National Cancer Institute's Urologic Oncology Branch is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize the use of Tempol to target HIF-2a in cancer.

Summary:

The National Cancer Institute (NCI) seeks research co-development partners and/or licensees to develop hetIL-15 in combination with other agents, such as PPARa agonists (Fenofibrate), FLT3 inhibitors (quizartinib), IL-12, or chemotherapy into a therapeutic for cancer.

Enterovirus D68 (EV-D68) has been linked to the widespread outbreaks of respiratory illness and acute flaccid myelitis (AFM) in the United States and Europe in 2014, 2016, and 2018. Although EV-D68 is now the most frequently encountered enterovirus (41.1% of cases), with an estimated global prevalence of 4%, there are no specific, FDA-approved therapeutic interventions targeting this virus.

Mesothelin (MSLN) is an excellent target for antibody-based therapies of cancer because of its high expression in many malignancies but lack of expression on essential normal tissues. Unfortunately, a large fragment of MSLN is shed from cancer cells, causing the currently available anti-MSLN antibodies (and immunoconjugates thereof) which bind to the shed portion of MSLN to quickly lose their therapeutic effectiveness over time. Indeed, the shed portion of MSLN can act as a decoy for these antibodies, further limiting them from reaching and destroying tumor cells.

This technology includes a micro-engineered “thyroid-on-a-chip” that combines human thyroid organoids with integrated micro-vasculature to replicate the gland’s native blood flow and 3-D architecture, enabling rapid, patient-specific drug screening. By permitting real-time perfusion of nutrients, hormones, and immune cells, the platform yields more physiologically relevant data than conventional static cultures or animal surrogates.

Up to 10% of the US population suffers from food allergies, with more than 40% of those experiencing life-threatening anaphylaxis. Peanut is one of the most common food allergens that give rise to persistent IgE-mediated food allergy. Oral immunotherapy (OIT) is used to reduce sensitivity to an allergen through repeated, small-dose exposure to the allergen. However, only a subset of patients develop a sustained response to the allergen and OIT carries notable side effects. 

This technology discloses the use of small-molecule iron chelators—drugs that bind and remove excess iron—for the oral treatment of developmental stuttering in children and adults. Mouse models carrying human stuttering mutations show both elevated striatal iron and impaired vocalization; daily low-dose deferiprone reverses these speech-like deficits while normalizing brain-iron MRI signals.