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Pan-SHIP1/2 inhibitors enhance phagocytosis of dead neurons and amyloid beta by microglia. Background: The beta-amyloid (1-42) peptide fragment is a crucial component of beta-amyloid debris that forms plaques in Alzheimer's Disease, playing a significant role in disease pathology and cognitive decline. Increased amyloid deposits and tau tangles exert chronic stress on microglia, leading to the emergence of "dark microglia" associated with pathological processes in Alzheimer's, including production of inflammatory cytokines, neurocytotoxicity, loss of neuronal synapses, and promotion of neuro-fibrillary tau tangles. However, microglia also have substantial homeostatic functions in the brain, which include pruning of synapses or phagocytic clearance of dead cells, cell debris, and beta-amyloid deposits. Technology Overview: The newly developed small molecule pan-SHIP1/2 inhibitors can modulate microglia activity in vivo, enhancing basal microglial homeostatic functions for therapeutic purposes in Alzheimer's disease. Specifically, the inhibitors, which were shown to be bioavailable in the central nervous system (CNS) in a mouse model, significantly increase phagocytosis of dead neurons and amyloid beta by microglia both in vitro and in vivo. The ability of these compounds to increase microglial and myeloid cell numbers in the CNS, while enhancing their capacity to remove beta-amyloid deposits, suggests that they could be used to reduce or reverse cognitive decline in Alzheimer's patients. Advantages:

• Bioavailability in the CNS
• Immunotherapeutic approach

Applications:

• Alzheimer’s disease
• Other dementias

Intellectual Property Summary: Patent application submitted,

• PCT/US2019/044476 Methods of activating microglial cells 
• EP3829589 Methods of activating microglial cells
• AU2019314405 Methods of activating microglial cells 
• CA3107823 Methods of activating microglial cells 
• U.S. 17/262,784 Methods of activating microglial cells

Licensing Potential: Development partner, Commercial partner, Licensing, Seeking investment Licensing Status: This technology is available for licensing. https://suny.technologypublisher.com/files/sites/istock-513688464.jpg  

Computationally predicts potential ideal interaction points for the molecular chaperone heat shock protein-90 (Hsp90). Background:
Molecular chaperones assist in the folding of unfolded and misfolded polypeptides by stabilization of folding intermediates and prevention of protein misfolding and aggregation. Molecular chaperones are present in all organisms and are essential for cell survival. The chaperone heat shock protein-90 (Hsp90) controls the folding of client proteins important for tumorigenesis. Hsp90 facilitates the maturation of substrates (or clients) that are involved in many different cellular pathways. Hsp90 clients include, among others, kinases, transcription factors, steroid hormone receptors and E3 ubiquitin ligases. The development of Hsp90 ATP-competitive inhibitors has been limited partly because it results in the simultaneous blockage of all clients, ultimately causing antiapoptotic heat shock response.Technology Overview:  
This technology computationally predicts the most unstable regions on the native structures of clients c-Abl, c-Src, Cdk4, B-Raf and Glucocorticoid Receptor, as potential ideal interaction points with the Hsp90-system. This enables researchers to synthesize peptide mimics spanning these regions and confirm their interaction with partners of the Hsp90 complex (Hsp90, Cdc37 and Aha1) by Nuclear Magnetic Resonance (NMR). Designed non-naturally occurring peptides selectively disrupt the association of their respective clients with the Hsp90 machinery, leaving unrelated clients unperturbed and causing apoptosis in cancer cells. Overall, selective targeting of Hsp90 protein-protein interactions is achieved without causing indiscriminate degradation of all clients, setting the stage for the development of therapeutics based on specific chaperone:client perturbation.
 https://suny.technologypublisher.com/files/sites/adobestock_4870932151.jpegAdvantages:  
•    Enables the development of therapeutics based on Hsp90.
•    Avoids antiapoptotic heat shock response.  Applications:  
The primary application for this technology is the development of therapeutics based on Hsp90.  Intellectual Property Summary:
PCT Nationalized, including US2021/0214734 and EP4090679Stage of Development:
TRL 3 - Experimental proof of concept Licensing Status:
This technology is available for licensing.Licensing Potential:
This technology would be of interest to anyone involved in the development of therapeutics based on Hsp90, including:
•    Pharmaceutical manufactures.
•    Hospitals.
•    Medical laboratories.
•    Universities.

­A killed ZIKA vaccine that prevents infection and is safe for pregnant women. Background:
Zika virus (ZIKV) is a Flavivirus transmitted by mosquitoes. First discovered in 1947, it remained a minor infectious entity until 2007, when the first large outbreak was reported in Micronesia. Subsequent severe outbreaks in French Polynesia (2013-14) and in Brazil (2015) put ZIKV on the map. Those outbreaks showed that Zika Virus is not only transmitted by mosquitos, but also by sexual contact and in utero, from Mom to fetus. While most people infected with ZIKV have few to no symptoms; the outbreak in Brazil was associated with increased microencephaly, with other severe congenital malformations, and with neurological complications.By 2016, 39 countries and territories in the Americas had confirmed local, vector-borne transmission of ZIKV as well as superinfection from one person to another. That, coupled with the severity of symptoms, triggered a campaign to create a robust ZIKV vaccine.Technology Overview:  
In a collaborative effort, scientists in the Army and at SUNY have created and tested a killed ZIKA vaccine. It has undergone Phase 1 and 2 testing in pregnant mouse and pregnant marmoset models. It has also been tested in humans.
Further Details:

1. Safety and immunogenicity of a Zika purified inactivated virus vaccine given via standard, accelerated, or shortened schedules: a single-centre, double-blind, sequential-group, randomised, placebo-controlled, phase 1 trial. Lancet Infect Dis. 2020 Sep;20(9):1061-1070. doi: 10.1016/S1473-3099(20)30085-2. Epub 2020 May 6. PMID: 32618279; PMCID: PMC7472641. (https://pubmed.ncbi.nlm.nih.gov/32618279/) 
2. Preliminary aggregate safety and immunogenicity results from three trials of a purified inactivated Zika virus vaccine candidate: phase 1, randomised, double-blind, placebo-controlled clinical trials. Lancet. 2018 Feb 10;391(10120):563-571. doi: 10.1016/S0140-6736(17)33106-9. Epub 2017 Dec 5. Erratum in: Lancet. 2020 Jun 20;395(10241):1906. PMID: 29217375; PMCID:PMC5884730. (https://pubmed.ncbi.nlm.nih.gov/29217375/) 
3. Sci Transl Med. 2017 Dec 13;9(420):eaao4163. doi: 10.1126/scitranslmed.aao4163. Erratum in: Sci Transl Med. 2018 Jul 18;10(450):PMID: 29237759; PMCID: PMC5747972. (https://pubmed.ncbi.nlm.nih.gov/29237759/)

https://suny.technologypublisher.com/files/sites/adobestock_1194681161.jpegAdvantages:  
•    Broad application  Applications:  
•    Prevention of ZIKV infection with a vaccine that is safe even for pregnant women.
 
Intellectual Property Summary: Zika virus vaccine and Methods of Production is protected by patent 11,033,615 which issued on June 15, 2021 https://patents.google.com/patent/US11033615B2/
Stage of Development:
TRL 4 – Technology validated in lab
Licensing Status:
This technology is available for licensing.
 

Targeted gene silencing technology promotes corneal wound healing. Background: Ocular scarring after surgery, trauma, or infection leads to vision loss and blindness. Blindness due to corneal scarring can currently only be resolved by transplantation, necessitating new approaches in regenerative wound healing in the eye.Technology Overview:  A self-deliverable siRNA has been developed by Upstate Medical University researchers to specifically target a gene that modulates scarring in order to promote corneal wound healing. The approach has been validated ex vivo and in vivo, with treatment after corneal wounding resulting in faster wound closure, limited scarring, suppression of fibrotic markers, and restoration of corneal thickness. https://suny.technologypublisher.com/files/sites/110-2089.jpghttps://www.pexels.com/photo/human-eye-2609925/Advantages:  

• Targeted siRNA therapy circumvents the need for immunologically compatible corneal donors.
• In vivo studies demonstrate this therapy promotes 41.5% reduction in scarring

  Applications:  

• Effective treatment for corneal scarring resulting from mechanical injuries, burns, infections or surgery.
• Model useful to study pathogenesis of fibrotic healing.

Licensing Status: Available for licensing or collaboration.