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A multi-disciplinary Institute within the University of Oxford which focuses upon translational activities to catalyse the discovery of new medicines.

What's next for Alzheimer's Disease

Inside Health reports on the latest advances in treating Alzheimer's disease, and the therapies being developed

Activation of SYK, a kinase implicated in Alzheimer’s disease

Publication explores the mechanism of activation of SYK upon phospho-ITAM binding through structures and biophysical measurements

Beyond lecanemab: unravelling the future of Alzheimer’s treatments

The latest Alzheimer’s treatments work by removing the build-up of a protein in the brain, called amyloid. But is this the only way we will treat the disease in the future?

First structure of amino acid transporter and viral receptor CAT1 determined at the CMD

Cationic Amino acid Transporter 1 (CAT1) imports basic amino acids and is also the receptor of two retroviruses. Our new structures of MmCAT1 reveal its amino acid selectivity, transport, and interactions with Friend Murine Leukemia Virus.

CMD study reports first chemical probe for CDKL2

Cyclin-dependent kinase-like 2 (CDKL2) is a serine/threonine kinase with reported links to development and cancer. A new study involving collaboration between the Bullock group at CMD Oxford and Alison Axtman at SGC-UNC reports the first chemical probe for CDKL2 providing an important reagent to interrogate CDKL2-dependent biology.

DPhil student Donna Di Rienzo is the recipient of an ARUK Thames Valley Pilot Project Award

This grant will launch an exciting collaboration with Dr Darragh O’Brien, Head of Structural and Mechanistic Proteomics, to run a ubiquitomic study to identify novel substrates of the E3 ligase IDOL, which is a promising therapeutic target for Alzheimer’s disease.

DPhil Student Matthew Holland Featured in Tatler Magazine after Presenting The Boat Race on BBC One

He finds parallels between explaining science and rowing. Both may seem complex at first, but breaking down basic principles can simplify understanding.

NLRP3 Inflammasome “DUBbed” by UCH-L1, affecting IL-1β production macrophages and microglia

Activation of the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome complex involves association with ubiquitin C-terminal hydrolase 1 (UCH-L1). UCH-L1 chemical inhibition and deletion interfere with NLRP3 assembly and IL-1β production in macrophages and microglia.

CMD Study Discovers Unexpected Noncovalent Off-Targets of Clinical BTK Inhibitors

BTK inhibitors are a cornerstone of clinical anticancer therapy thanks to their strong and sustained effect on key disease-driving oncogenes. A new study by the Huber lab in collaboration with the Brennan and Fedorov groups at CMD, as well as Ivan Ahel’s lab at the William Dunn School at Oxford, reveals that these drugs exhibit unexpected off-target activity against non-kinase proteins that is independent of their reactive warhead.

Discovery of Conformationally Constrained ALK2 Inhibitors

The Bullock's lab, in collaboration with Ontario Institute for Cancer Research (OICR) and M4K Pharma, has published a study in the Journal of Medicinal Chemistry about the discovery of conformationally constrained ALK2 inhibitors.

Research team receives $25m Cancer Grand Challenges award

A global, interdisciplinary team of researchers, including the Centre for Medicines Discovery’s Professor Frank von Delft, has been selected to receive a Cancer Grand Challenges award of up to $25m over five years to tackle the solid tumours in children challenge. The Cancer Grand Challenges PROTECT team is led by Professor Stefan Pfister of the Hopp Children's Cancer Center in Heidelberg.

ASAP Discovery Consortium wins 2023 FASEB Dataworks prize

The AI-driven Structure-enabled Antiviral Platform (ASAP) has won an Exemplary Achievement Award from the Federation of American Societies for Experimental Biology (FASEB) and the National Institutes of Health (NIH). The prize recognises data practices in biological and biomedical research labs during the active phase of research.

Alzheimer’s disease: Protein-protein interaction inhibitors for MSN and CD44

Researchers have delved into developing small molecule inhibitors targeting protein-protein interactions in Alzheimer's disease.

The C2 domain of SHIP1 as an allosteric modulator of phosphatase activity

Publication explores the mechanism by which the C2 domain of SHIP1 is able to modulate inositol 5-phosphatase activity, providing insights into potential methods of targeting the protein to understand its role in Alzheimer’s disease.

Latest research at CMD identifies mutations in the BTB domain of KCTD15 that perturb BTB oligomerisation and cause a distinctive frontonasal dysplasia syndrome

Study identifies de novo missense variants in KCTD15 associated with frontonasal mass phenotype.

The solute carrier SPNS2 recruits PI(4,5)P2 to synergistically regulate transport of sphingosine-1-phosphate

The Dürr and Sauer group's new publication reveals export of immunoregulatory sphingosine-1-phosphate is regulated by the signaling lipid PIP2 via its action on the transporter SPNS2.

Discovery of a chemical probe for CDKL5 demonstrates role in hippocampal CA1 physiology

Mutations in CDKL5 cause a severe neurodevelopmental disorder. A recent paper in eLife reports the first chemical probe for CDKL5 that reveals new insights into the roles of CDKL5 in synaptic plasticity and human neuropathology.

Research reveals basis for KEAP1-CUL3 E3 ligase assembly and inhibition by CDDO

Bullock group's recent paper uncovers structural basis for KEAP1 assembly with CUL3 and offers a new generalizable TR-FRET assay platform that defines the contributions of different domains to their binding affinity.

Research reveals the first molecular understanding of BIRC6 – an essential regulator of cell death

Latest research has uncovered at the molecular level how BIRC6 (a giant ubiquitin ligase) keeps cells alive.

FOP Friends lab visit

The Bullock group was delighted to welcome the FOP Friends charity and patient families to the CMD in October. FOP (fibrodysplasia ossificans progressiva) is a congenital syndrome of extraskeletal bone formation caused by a gain of function mutation in the ACVR1/ALK2 protein kinase. Families were given a lab tour and updated on the latest research news, including progress of the “STOPFOP” clinical trial developed by the Bullock group and collaborators.

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