Main Menu

Adenosine modulates many physiological processes by activating specific adenosine receptors. These adenosine receptors play a critical role in the regulation of cellular signaling and are broadly distributed throughout the body. Thus, the ability to modulate adenosine receptor-mediated signaling is an attractive therapeutic strategy for a broad range of diseases. This technology relates to a group of compounds that display high affinity and specificity for the A1 adenosine receptor subtype.

The invention is directed to modification of a particular sugar by the enzyme arylsulfatase B (ARSB), which results in axon regeneration.

There is no vaccine for malaria, and there is growing resistance to existing anti-malarial drugs. Sexual stage-specific antigens are of interest as vaccine candidates because disruption of these antigens would reduce the fertility and, thus, the infectivity of the parasite.

The invention pertains to derivatives of docosahexaenoylethanolamide (synaptamide or DEA) and their use in inducing neurogenesis, neurite growth, and/or synaptogenesis. As such, these DEA derivatives can be used as therapeutics for neurodegenerative diseases such as traumatic brain injury, spinal cord injury, peripheral nerve injury, stroke, multiple sclerosis, autism, Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis. The DEA derivatives of the invention have increased potency and hydrolysis resistance as compared to native DEA.

Available for licensing are inhibitors that target the USP1/ UAF1 deubiquitinating enzyme (DUB) complex. The FDA approval and commercial success of Velcade®, a small molecule proteasome inhibitor, has established the ubiquitin-proteasome system (UPS) as a valid target for anticancer treatment. However, proteasome inhibitors in general suffer from a narrow therapeutic index and acquired resistance. A promising alternative to proteasome inhibition has been to target the enzymes upstream of proteasome-mediated protein degradation, i.e.

Five human induced pluripotent stem cells (iPSC) lines are generated using lentivirus-based reprogramming technology. These lines are pluripotent, meaning they have the potential to differentiate into all cells in the body, and theoretically can proliferate/self-renew indefinitely. The iPSC lines are: NC1 (derived from female's fibroblasts), NC2 (derived from female's fibroblasts ), NC3 (derived from male's HUVECS), NC4 (derived from male's fibroblasts) and NC5 (derived from female's fibroblasts). Further details of these cells are available upon request.

This technology describes the use of novel mutated anthrax protective antigen (PA) protein variants to target tumor cells and tumor vasculature. NIH scientists have engineered two PA variants that selectively complement one another and combine to form active octamers that target tumor cells. This controlled oligomeric activation of the PA proteins makes the likelihood of toxicity to non-tumor cells very low since non-tumor tissue does not express certain cell-surface proteases required to activate the PA variants.

Q490L point mutation was introduced into the rat M3 muscarinic receptor cDNA to confer persistent, constitutive (ligand-independent) activity. Expression of the M3 receptor mutant was placed under the control of a 650 bp fragment of the rat insulin promoter II (RIP II) to limit expression to the islet beta cell.

Researchers at NIH have developed islet beta cell M3 muscarinic acetylcholine receptor knockout mouse. The mice were generated by crossing floxed mouse M3 muscarinic acetylcholine receptor mice with mice in which Cre recombinase was controlled by the beta-cell specific rat insulin promoter (RIP-Cre mice).

Researchers at NIH have generated transgenic mice in which the M3 muscarinic receptor is overexpressed in pancreatic beta cells. This was done by placing the receptor gene under the control of the 650 bp rat insulin promoter II (RIP II). The resulting mice show a pronounced increase in glucose tolerance and enhanced plasma insulin levels. Strikingly, these mutant mice were resistant to diet-induced glucose intolerance and hyperglycemia.