Suchismita Acharya PhD
Our laboratory is in the North Texas Eye Research Institute at the University of North Texas Health Science Center. Our current research is focused on expanding the chemical toolbox for neural signaling and anti-inflammation/anti-oxidant pathways to understand the mechanism of action of the disease pathology associated with glaucomatous optic neuropathy, Alzheimer Diseases, Ischemic stroke as well as angiogenesis. Our lab integrates medicinal chemistry, chemical biology, bio-engineering, and drug delivery via nanotechnology. We employ synthetic organic and organometallic chemistry to generate small molecule library for low throughput as well as high throughput screening (target based as well as phenotypic). We have projects involving traditional medicinal chemistry SAR for property optimization to find hit to lead and structure, fragments or ligand based drug design using structural biology, and computational chemistry tools. Fluorescent and ESR active probe design for signaling study as well chemoluminoscense assay is used in our group. Pro-drug design to achieve chemical and metabolic stability, use of nanomeric materials and polymeric particles for drug delivery study is another core interest.
- Glaucomatous optic neuropathy:Primary open angle (POAG) glaucoma is associated with elevated intraocular pressure and progressive neurodegeneration of retinal ganglion cells (RGCs). Nitric oxide has potential to reduce IOP with possible neuroprotective activity, however, superoxide radicals generated during optic neuropathy may deplete the NO (nitric oxide) bioavailability. We are designing, synthesizing library of robust nitric oxide donor in combination with antioxidant functional group that will improve the nitric oxide bio-availability necessary for lowering IOP with possible neuroprotection potential. This may lead to development of a new class of hybrid molecules for the treatment of glaucomatous optic neuropathy.
Age related macular degeneration and retinopathy:
Multiple lines of evidence suggest that, Toll Like Receptor 4 (TLR4) signaling may be associated with pathologic changes in retinal diseases, including age related macular degeneration (AMD) eyes by oxidized lipids, lipofuscin and by drusen components. Once activated, TLR4 could contribute to the pathogenesis of AMD by multiple mechanisms such as release of TNF-α, interleukin-1β, and other pro-inflammatory mediators, photoreceptor outer segment membrane recognition, oxidant production, and LPS recognition. Release of high-mobility group box-1 (HMGB1) in ischemic neural tissue has been shown to initiate TLR4-dependent responses that contribute to retinal neovascularization. Therefore, inhibition of TLR4 activity may be of therapeutic value in AMD and other retinal diseases. For that purpose, we are specifically interested in studying the structure activity relationship of small molecular weight, non-toxic natural products and analogs as TLR4 antagonists.
This page was last modified on October 10, 2019