Jon (Jed) Chatterton Email & Phone Number

Malvern, Pa, Us

Philadelphia, Pa, Us

Philadelphia, Pa, Us

I led a team developing gene therapy vectors for complement factor H (CFH) expression in the treatment of geographic atrophy.

Cambridge, Massachusetts, Us

I led a team developing methods for delivery of non-viral gene therapy vectors to the retina using AAV as a benchmark. I also worked cross-functionally with Hepatic Delivery and Formulations Teams to enhance ctLNP platform.

Durham, North Carolina, Us

I led a team expanding therapeutic use of novel gene editing platform to ophthalmic indications. I also collaborated with the Cell Therapy Team to inhibit host immune response to “off-the-shelf” CAR-T cells.

I led and managed discovery and development of nucleic acid-based therapeutics for ophthalmic disease.

Chicago, Il, Us

I provided expert scientific advice on drug targets, delivery technology, imaging methods, biomarkers, and pre-clinical/clinical data in support of strategic planning, due diligence, and portfolio management in ophthalmology.

Dublin, Coolock, Ie

I led a team of scientists in developing novel, translatable animal models of retinal disease and in performing in vivo target validation to support the biologics program.

Geneva, Switzerland, Ch

I established therapeutic siRNA program at Alcon, addressing targets in age-related macular degeneration (AMD), diabetic macular edema, glaucoma, allergy, and dry eye. I led two multi-disciplinary teams in a matrixed environment, one developing a ligand-siRNA conjugate as a clinical candidate for treatment of AMD, and the second performing assay development, target validation, and compound screening for ocular adenoviral infection. I initiated and managed 7 external collaborations on screening and in vivo delivery of siRNAs against 20 therapeutic targets, and two collaborations on identifying new drug targets in glaucoma and AMD.

Geneva, Switzerland, Ch

Us

I led a team of scientists in development and use of siRNA technology for target identification and validation in neurodegenerative disease, cancer, metabolic disease, and infectious disease. Our results included identification and validation of four potential drug targets.

La Jolla, Ca, Us

• Cloned and characterized NR3B (aka GRIN3B), the final member of the NMDA receptor family. NR3B co-assembled with NR1 to form glutamate-insensitive, excitatory glycine receptors with properties distinct from those of classical NMDA receptors.• Knockout of membralin resulted in early-onset motor neuron disease in mice. Loss of membralin function attenuated ER-associated protein degradation and induced ER stress, suggesting that membralin plays a critical role in motor neuron survival. • Designed, constructed, and packaged lentiviral vectors for transduction of cultured neurons and delivery to rodent CNS

Cambridge, Ma, Us

• Cloned the LDLB gene, which rescued ricin-hypersensitivity and LDL receptor-deficiency in ldlB cells, using a retroviral vector-based cDNA library. Demonstrated that LDLB encodes a component of a protein complex, COG, required for normal Golgi function and membrane traffic. • Performed single-molecule electron microscopy of SR-AI and SR-AII macrophage scavenger receptor extracellular domains, which confirmed the predicted structure and suggested a possible structure-function relationship

Los Angeles, Ca, Us

• ApoB polymorphism effects on LDL metabolism using biophysical methods. The apoB R3531C polymorphism contributes to hypercholesterolemia and premature atherosclerosis, while six common apoB polymorphisms have little, if any, effect

Taught Organic Chemistry on weekends at the Whittier, California campus.

Doctor Of Philosophy (Ph.D.), Biochemistry

B.S., Biochemistry