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This technology includes a family of transcatheter endovenous intramyocardial tether (MIRTH) procedures to impose myocardial constraint on the LV (MIRTH), LV and RV (SCIMITAR), and cardiac resynchronization procedures. Included is a set of advanced cardiac treatment technologies that focus on minimally invasive procedures for heart patients. The main technology is the transcatheter endovenous intramyocardial tether (MIRTH) procedure, which is designed to apply physical constraint to the left ventricle (LV) of the heart.

This technology includes a novel transcatheter repair for functional mitral valve regurgitation, called mitral cerclage annuloplasty. This includes coronary artery protection for mitral cerclage annuloplasty against inside-out compression from subsequent transcatheter valve-in-ring mitral valve implantation, wherein the ring is created by the cerclage annuloplasty. Cerclage annuloplasty is to create a semi-rigid ring at the level of the mitral annulus.

This technology includes a metallic guidewire that is suitable for MRI catheterization, because it is mechanically long but electrically consists of short conductive segments that cannot resonate during MRI. The invention consists of stiffness-matched non-conductive connectors or connections that are used along with short metallic segments. The embodiment reduced to practice has torquability and flexibility comparable to marketed metallic guidewires, yet is free from MRI heating.

This technology includes a catheter design to be used for cardiovascular procedures. This catheter has intrinsic freedom from MRI heating by segmenting and insulating the braiding material, yet that retains most of the mechanical properties of a braided catheter aligning the segment interruptions out-of-phase with each other.

This technology includes a guidewire purpose-built for delivery of bulky transcatheter heart valves (THV). Conventional THV guidewires are rigid and have a distal tip shaped like a pigtail to prevent apical ventricular perforation. This invention is a 3-dimensional helical or antihelical curve that can protect against apical perforation, possibly better, and that allows subtle 3-mensional deflection to aid the operator in achieving coaxiality or overcoming delivery obstacles such as calcific spicules.

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.

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.