This technology includes a catheter-delivered endograft designed to treat congenital heart disease without surgery. The specific surgical procedure averted is cavopulmonary bypass graft. The key innovations are features to effect distal end-to-side anastomosis and proximal end-to-end anastomosis without surgery. The system operates under X-ray and MRI guidance.
This technology includes the combination of a kinase inhibitor (specifically ibrutinib) with a bispecific antibody (specifically a CD19/CD3 bispecific antibody) to be used to treat cancer. CD19/CD3 bispecific antibodies (bsAbs) can be used to recruit endogenous T cells against CD19+ tumor cells via the formation of cytolytic synapses. lbrutinib, a BTK inhibitor, has been shown to normalize T cell dysfunction characteristic of CLL.
This technology includes monoclonal antibodies (mAb) that specifically and with high affinity bind the final complement components C3dg and C3d (subsequently referred to as C3d), which can be used to kill tumor cells that carry C3d on their cell surface. We show that tumor cells of patients treated with the therapeutic anti-CD20 mAb ofatumumab carry C3d on the cell surface and can bind and be killed by addition of anti-C3 mAbs. In contrast, further addition of more ofatumumab has only minimal effects.
The HEK293T/T7 cell line is a novel development in virology research, particularly for studying human noroviruses. This cell line expresses the T7 RNA polymerase, a key enzyme used in reverse genetics systems. Unlike existing technologies, the HEK293T/T7 cell line offers the unique advantage of being able to produce functional T7 RNA polymerase, which is essential for driving transcription from T7 promoters.
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:
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:
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.
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.
This technology involves an innovative method for differentiating neural stem cells (NSCs) into neurons, primarily for use in basic science research and in developing therapies for brain and spinal cord disorders. Existing methods for generating neurons from NSCs typically result in high efficiency but low survival rates, especially when neurons are dissociated and regrown. This new method utilizes Life Technologies StemPro embryonic stem cell serum-free medium, which significantly enhances differentiation efficiency into neurons with minimal cell death.