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Building on the unique disease physics/tissue transport enabled by high hydroxyl densities on dendrimers, more than 8 years ago, our group designed, developed, and patented glucose-based dendrimers and DDCs to engineer interactions with dysregulated glucose metabolism on injured neuronal cells.

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Our recent innovation, using nanoscale biophysics, is the glucose dendrimer (GD2) platform. These dendrimers are designed take advantage of the surface OH groups to navigate to navigate the brain’s intricate architecture, interacting with glut receptors and glucose transporters on dysregulated neuronal cells and adipocytes. This allows us to deliver drugs and genes specifically to injured neuronal cells, with transformative implications for neurological, pain and depression disorders.

  • Selective and Precise: GD2 robustly accumulates in overactive neurons while avoiding non-excitable or resting cells, ensuring unparalleled targeting accuracy.
  • Activity-Dependent Uptake: Neuron entry is driven by activity, meaning GD2 responds dynamically to disease-relevant hyperexcitability.
  • Versatile Delivery: The platform can be conjugated with different drugs and delivered through different administration routes for rapid, noninvasive brain access.

This ligand-free and scalable system represents a paradigm shift in precision nanomedicine. It offers modular flexibility to deliver anticonvulsants, neuroprotectants, and neuromodulators for a wide range of central nervous system (CNS) disorders marked by neuronal hyperexcitability, including epilepsy, traumatic brain injury, and neurodegeneration.

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References:

  1. Sharma AS, Sah N, Sharma R, Vyas P, Liyanage W, Kannan S*, Kannan RM*, “Development of a novel glucose-dendrimer based therapeutic targeting hyperexcitable neurons in neurological disorders. Bioengg. and Trans Medicine. 2024: 9(5), e10655.
  2. US Patent #18/854,897, Dendrimer compositions for targeted delivery of therapeutics to neurons, Kannan Rangaramanujam, Rishi Sharma, Sujatha Kannan, Anjali Sharma, Nirnath Sah, Mira Sachdeva, Siva Kambhampati, 4/2024.