The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a class of novel aplithianine-derived small molecule analogs that compete with ATP for binding on a range of clinically relevant kinases including:
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for a class of novel aplithianine-derived small molecule analogs that compete with ATP for binding on a range of clinically relevant kinases including:
This technology includes a new chemical scaffold (with lead compound XL5) against hRpn13 that induces apoptosis, which may have clinical efficacy against cancer. The structure of XL5-conjugated hRpn13 guided the design of XL5-PROTAC degrader compounds that exhibit greater efficacy than previous hRpn13-targeting compounds, as evaluated by selectivity for hRpn13, induction of apoptosis, and loss of cell viability. In cells, XL5-PROTACs revealed the presence of a truncated hRpn13 product that binds to proteasomes and is selectively degraded by XL5-PROTACs.
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for Chimeric VLP Vaccines to Prevent HTLV-1 Infection.
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for viral peptide (CE1)-based therapeutics for HCC prevention and treatment.
Summary:
The National Cancer Institute (NCI) seeks research co-development partners and/or licensees for three small molecules that target hRpn13, an overexpressed protein in certain cancers.
Description of Technology:
The National Cancer Institute (NCI) sees research co-development partners and/or licensees for an automated acoustophoresis device to radio-label and isolate cells.
The National Cancer Institute (NCI) seeks research co-development partners and licensees for a panel of five fully human antibodies against CD276 for the treatment of solid tumors. The collection also includes human CARs incorporating the antibodies for immunotherapeutic use.
Immune checkpoint inhibitors (ICIs) vastly improved the outcome of various advanced cancers; however, many are less likely to respond to single-agent ICI. Tumors with low T-cell infiltration are "immunologically cold" and less likely to respond to single-agent ICI therapy. This diminished response is presumably due to the lack of neoantigens necessary to activate an adaptive immune response. On the other hand, an "immunologically hot" tumor with high T-cell infiltration has an active anti-tumor immune response following ICI treatment.
Cancer cells may acquire drug resistance after prolonged chemotherapy. In many cases, cancer cells develop resistance to several drugs with distinct structures and modes of action. This multi-drug resistance phenomenon increases the complexity of cancer treatment.