Lindon Moodie

Universitetslektor vid Institutionen för läkemedelskemi; Läkemedelsdesign och läkemedelsutveckling

E-post:: lindon.moodie@ilk.uu.se
Besöksadress:: Biomedicinskt Centrum BMC, Husargatan 3
Postadress:: Box 574
751 23 UPPSALA

Ladda ned kontaktuppgifter för Lindon Moodie vid Institutionen för läkemedelskemi; Läkemedelsdesign och läkemedelsutveckling

ORCID:: 0000-0002-9500-4535

Kort presentation

Assoc. Sen. Lecturer (Biträdande Lektor) at the Department of Medicinal Chemistry, affiliated with the Uppsala Antibiotic Centre. After training as a synthetic organic chemist, I became interested in applying these skills towards solving biological problems. Particularly interested in antibiotic discovery and exploring how small molecules influence both the human microbiome and host physiology.

Nyckelord

Biografi

Born in Ashburton, New Zealand, Lindon studied chemistry at the University of Otago, Dunedin, New Zealand. Working under the supervision of Professor Dave Larsen, he obtained his PhD in 2013 where his research focused on natural product total synthesis and methodology development. He then joined the groups of Assoc. Prof. Johan Svenson and Assoc. Prof. Jørn Hansen at The University of Tromsø - The Arctic University of Norway. Here, he employed natural product scaffolds as inspiration to combat marine biofouling, and developed marine natural products as acetylcholinesterase inhibitors. In 2015, Lindon relocated to Umeå University, Sweden (Assoc. Prof. Christian Hedberg), where he investigated the interplay between bacterially derived small molecules and the human host.

Lindon joined the Department of Medicinal Chemistry at Uppsala University in April 2019 as an Assoc. Sen. Lecturer (Biträdande Lektor), affiliated with the Uppsala Antibiotic Centre.

Forskning

Lindon aims to employ synthetic organic chemistry and chemical biology as tools to interrogate how relevant small molecules influence both host and bacterial physiology. The information gained will guide the development of novel antibiotic classes and will enable new modalities to selectively edit the human microbiota of infection and disease causing bacteria.