Laura Bohn
Northeastern University, MA·Pharmacology
The body makes its own cannabis-like molecules, and these act on two receptors, CB1 and CB2, that sit on the surface of nerve and immune cells. Drugs aimed at this system could treat pain, but almost none have become safe, approved medicines: compounds that activate CB1 directly tend to cause unwanted effects, tolerance, and dependence.
- Fields
Pharmacology
Neuroscience
Biochemistry
- Topics
cannabinoid receptors
endocannabinoid system
biased agonism
- Grants
- 1 known grant, through May 2027
What they work on
- Define the whole-animal pharmacology of functionally selective CB1 agonists, compounds that activate only some of the receptor's signaling routes, measuring cardinal signs of CB1 activation, suppression of nerve-injury pain, tolerance and physical dependence.
- Test slowly dissociating, tight-binding and probe-specific CB1 positive allosteric modulators, which bind away from the usual drug pocket to tune the receptor, for potency and side-effect liability in vivo.
- Determine whether agonists with high affinity for CB2 and little activity at CB1 give improved in vivo profiles, comparing cannabis-like effects, relief of touch-evoked pain, tolerance and dependence.
- Test whether combining CB1 blockade - neutral antagonism, inverse agonism or partial agonism - with high-affinity CB2 activation in a single ligand improves efficacy while limiting dependence and negative affective states.
More about the research
Part of the problem is that a receptor does not send a single message. The same receptor can trigger several internal signaling routes, and which route matters for pain relief versus which causes side effects is still poorly understood. Closing that gap is the point of this work.
Why it matters
Cannabinoid receptors are promising pain targets, but candidate drugs have repeatedly failed between the laboratory and the clinic because side effects, tolerance and dependence travel with pain relief. Separating the receptor signaling routes that relieve nerve-injury pain from those that cause harm would give drug developers a clear readout to aim at, which could reduce costly clinical failures and eventually support safer cannabinoid-based treatments for chronic pain.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Mahmoud Ahmed
Texas Tech University Health Sciences Center, TX·Pharmacology
Develop new small-molecule inhibitors of the EphB1/2 tyrosine kinases, nerve-signaling enzymes, that are unrelated to tetracyclines, and define the structure–activity features needed for potent inhibition.
J McIntosh
University of Utah, UT·Pharmacology
Build a library of selective probes for nicotinic acetylcholine receptor subtypes that lack them, by mining cone snail venom peptides and refining them through structure-activity relationship studies.
Jerri Rook
Vanderbilt University, TN·Pharmacology
Test whether positive allosteric modulators of the M1 muscarinic receptor induce long-term depression of excitatory synapses by acting on M1 in prefrontal cortex pyramidal cells, and whether this requires phospholipase D rather than M1 in inhibitory neurons.
The school
Northeastern University: 27 labs on PI Pages, $347M a year on research, 251 research doctorates a year.
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