Thalidomide and its derivates induce degradation of many C₂H₂ zinc-finger transcription factors, including SALL4, providing insight into a long-standing mystery in modern pharmacology, and starting points for future drug development.

A transcription factor called SALL4 could be the missing link between thalidomide and the limb defects caused by the drug.

Careful analysis of adverse drug reaction reports reveals noise and biases embedded in this data and allows for systematic mitigation of these effects to produce much more robust understanding of side effects of marketed drugs.

The new drug 3,6’-dithiopomalidomide mitigates key markers of neuronal death and neuroinflammation and improves acute behavioral outcome measures in traumatic brain injury, a common, debilitating disorder that lacks effective treatment.

Cereblon-based small-molecule degraders rely on the sequential action of ubiquitin-conjugating enzymes UBE2G1 and UBE2D3 to assemble K48-linked polyubiquitin chains on cereblon neomorphic substrates, resulting in their proteasomal degradation.

High-throughput phenotypic screening followed by unbiased target identification reveals a new molecular glue HQ461 that induces CDK12-DDB1 interaction to promote degradation of Cyclin K via the ubiquitin proteasome system.

AirID provides highly interaction-dependent biotinylation for analysis of protein–protein interaction.

Operant drug self-administration in a mouse model of neuropathic pain reveals pain-relieving effects of a cannabinoid CB₂ receptor agonist that are mediated through CB₂ receptors of neurons and lymphocytes.