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Small Molecule Anti-cancer Agents that Stabilize the MYC-G-Quadruplex

The proto-oncogene c-Myc is deregulated and overexpressed in ~70% of all cancers. Thus, c-Myc is an attractive therapeutic target. Beyond cancer, Myc is also a positive effector of tissue inflammation, and its function has been implicated in the pathophysiology of heart failure. Researchers at the National Cancer Institute (NCI) developed novel small molecules that target c-Myc at the transcriptional level, thus enabling a potential pan-cancer therapeutic. Specifically, these compounds stabilize the transcription repressing quadruplex in the c-Myc gene promoter region. The National Cancer Institute seeks parties interested in licensing or collaborative research to co-develop these therapeutic targets.'

Combination Cancer Therapy with HDAC Inhibitors

NCI researchers developed a combination therapy of histone deacetylase (HDAC) inhibitors and immunotherapies, such as checkpoint inhibitors, virus-based vaccines, monoclonal antibodies, cell-based treatments or radiopharmaceuticals. The NCI Laboratory of Tumor Immunology and Biology seeks parties to license or co-develop this method.

Sensitizing Cancer Cells to DNA Targeted Therapies

Chk2 is a protein kinase activated in response to DNA double strand breaks. In normal tissues, Chk2 phosphorylates and thereby activates substrates that induce programmed cell death, or apoptosis, via interactions with p53, E2F1, PML proteins. In cancer tissues, where apoptosis is suppressed, Chk2 phosphorylates and inactivates cell cycle checkpoints (via interactions with Cdc25, phosphatases and Brca1 proteins), which allows cancer cells to repair and tolerate DNA damage. Hence, Chk2 inhibitors would be expected to protect normal tissues by reducing apoptosis, and to sensitize cancer cells to DNA-targeted agents. The National Cancer Institute seeks licensees for small molecule inhibitors of Chk2 for the treatment of cancer.

NSAIDs that Assist the Treatment of Human Diseases

Researchers at the National Cancer Institute (NCI) developed compounds containing both a non-steroidal anti-inflammatory drug (NSAID) and a nitroxyl (HNO) -releasing agent that have significantly reduced toxicity, allowing their use for extended periods of time without severe side effects.The HNO-releasing moiety contained in this invention may expand the medical utility of NSAIDs. HNO releasing agents possess anticancer activity as well as good antioxidant properties, which has potential benefit for a variety of human diseases, including acute and chronic inflammation. NCI seeks parties to license or co-develop this technology.

T Cell Receptors Targeting KRAS Mutants for Cancer Immunotherapy/Adoptive Cell Therapy

Researchers at the National Institutes of Health identified a collection of TCRs that exclusively recognize the common hotspot driver mutations in KRAS antigen, expressed by a variety of epithelial cancers, including pancreatic, colorectal and lung cancer. The mutated KRAS variants are recognized by the TCRs in the context of specific Class I/Class II HLA alleles. These TCRs can be used for a variety of experimental therapeutic, diagnostic and research applications.

Schweinfurthins and Uses Thereof

Researchers at the National Cancer Institute (NCI) developed novel analogs of the natural product schweinfurthins to treat neurofibromatosis type 1 (NF1). The compounds demonstrate effective growth inhibition in malignant peripheral nerve sheath tumor cell lines and mouse models of astrocytomas. Researchers seek licensing and/or co-development research collaboration opportunities to further develop the schweinfurthin analogs.

Methods of Producing Effective T-cell Populations Using Akt Inhibitors

Adoptive cell therapy uses cancer reactive T-cells to effectively treat cancer patients. Producing many persistent T-cells is critical for successful treatments. Researchers at the NCI seek licensing and/or co-development research collaborations for a novel method of producing effective T-cell populations using Akt inhibitors.

Peptide Mimetic Ligands of Polo-like Kinase 1 Polo Box Domain

Researchers at the National Cancer Institute (NCI) have developed peptidomimetic inhibitors that disrupt Polo-like kinase 1 (Plk1)-mediated protein interactions by targeting polo-box domain (PBD). The compounds are designed to selectively cause mitotic arrest in cancer cells with abnormal Plk1 expression. Researchers seek licensing and/or co-development research collaborations to further develop the inhibitors.

Peptide Mimetic Ligands of Polo-like Kinase 1 Polo Box Domain (“Plk1 PBD Portfolio”)

Researchers at the National Cancer Institute (NCI) have developed peptidomimetic inhibitors that disrupt Polo-like kinase 1 (Plk1)-mediated protein interactions by targeting polo-box domain (PBD). These compounds are designed to selectively cause mitotic arrest in cancer cells with abnormal Plk1 expression. Researchers seek licensing and/or co-development research collaborations to further develop the inhibitors.

Cancer-reactive T cells from Peripheral Blood

T-cells capable of reacting to mutations in cancer patients have potential use as therapeutics. Identifying and isolating these cells from patients is a crucial step in developing these treatments. Researchers at the National Cancer Institute (NCI) have developed a novel method of isolating mutation-reactive T-cells from a patient’s peripheral blood lymphocytes (PBL). The NCI, Surgery Branch, is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize this method of isolating mutation-reactive T-cells from peripheral blood.

Fully-human Heavy-chain-only Anti-B-cell Maturation Antigen (BCMA) Chimeric Antigen Receptors (CARs)

Chimeric Antigen Receptor T cell (CAR-T) therapies that specifically target B-cell maturation antigen (BCMA) are strong therapeutic candidates for patients with plasma cell malignancy diseases such as, multiple myeloma (MM), as well as for patients with Hodgkin’s lymphoma. BCMA is a cell surface protein preferentially expressed on a subset of B cells and mature plasma cells, but not on other cells in the body. The limited expression of BCMA on B and plasma cells makes BCMA an attractive therapeutic target for B cell and plasma cell malignancy diseases. The 12 anti-BCMA CARs described are fully human CARS and have the potential to treat patients with various plasma cell and B cell malignancy diseases.

Polymeric Delivery Platform for Therapeutics

The National Cancer Institute (NCI) seeks licensing and/or co-development research collaborations for a polymeric drug delivery platform that targets scavenger receptor A1 (SR-A1), a receptor highly expressed in macrophages, monocytes, mast cells, dendritic cells (myeloid lineages), and endothelial cells. The platform delivers various immunomodulatory therapeutic cargo including small molecule drugs, therapeutic peptides, and vaccines, to the lymphatic system and myeloid/antigen presenting cell (APC) sub-populations.

Overexpression of Phf19 on T Cells Enhances Therapeutic Effects of T Cell-Based Therapies (such as Chimeric Antigen Receptor [CAR] Therapies)

Researchers at the National Cancer Institute (NCI) have developed a method to epigenetically reprogram CD8+ T cell fate by expressing elevated levels of the polycomb-like protein, Phf19. This technology is useful for improving T cell-based immunotherapies (such as CAR therapies) to treat a range of infectious diseases and cancers. NCI seeks licensing or co-development partners for this invention.

Novel Murine T-Cell Receptors for Treating Metastatic Thyroid Cancer

Metastatic thyroid cancer can be resistant to current treatment options such as radioactive iodine therapy. Targeting thyroglobulin, a thyroid-specific antigen, as part of an adoptive cell therapy approach will allow for new therapeutic possibilities. Researchers at the National Cancer Institute (NCI) seek licensing and/or co-development research collaborations for novel T-cell receptors for the treatment of metastatic thyroid cancer.

Inhibition of T Cell Differentiation and Senescence by Overexpression of Transcription Factor c-Myb

Researchers at the National Cancer Institute (NCI) have developed a method by which memory T cells can be generated from other T cell populations using overexpression of the transcription factor c-Myb. Importantly, these reprogrammed memory T cells show increased proliferative and survival capacity. This strategy could also potentially generate anti-tumor T cells with improved viability and therapeutic efficacy for adoptive ACT. Researchers at the NCI seek licensing and/or co-development research collaborations for this invention.

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