Mahmoud Ahmed
Texas Tech University Health Sciences Center, TX·Pharmacology
Chronic pain from nerve damage is often treated with rising doses of opioids, feeding an overdose crisis that killed more than 107,000 people in the U.S. over one year.
- Fields
Pharmacology
Chemistry
Neuroscience
- Topics
neuropathic pain
chronic pain
EphB1
- Grants
- 1 known grant, through Feb 2030
What they work on
- 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.
- Determine in mouse models of nerve injury whether lead EphB1/2 inhibitors reverse or block thermal hyperalgesia (heat oversensitivity) and mechanical allodynia (touch-evoked pain).
- Uncover how the lead EphB1/2 inhibitors reduce neuropathic pain in mice, including their effects on peripheral and central nervous system neuron activation and pain-related biomarkers.
More about the research
Safer, non-addictive pain drugs are urgently needed. One candidate target is EphB1, an enzyme called a tyrosine kinase that relays signals in nerve cells. Earlier studies showed that mice lacking EphB1 no longer developed heightened pain after a sciatic nerve injury.
Why it matters
Peripheral neuropathic pain often leads to escalating opioid prescriptions. Potent, selective EphB1 kinase inhibitors could become a foundation for non-opioid, non-addictive treatments for people with chronic nerve-damage pain. This could help reduce reliance on opioids.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Bin Pan
University of Texas Medical Branch at Galveston, TX·Neuroscience
Establish whether CaMKII activity in peripheral sensory neurons suppresses pain, testing the hypothesis that reduced CaMKII signaling in dorsal root ganglion neurons maintains chronic pain in preclinical neuropathic and osteoarthritic pain models.
Kevin Tidgewell
University of Kentucky, KY·Pharmacology
Isolate bioactive compounds from Cameroonian medicinal plants such as Paullinia pinnata by fractionating extracts and testing each fraction for binding to sigma-2/TMEM97, a calcium-regulating protein linked to pain.
The school
Texas Tech University Health Sciences Center: 2 labs on PI Pages, $53M a year on research, 128 research doctorates a year.
Reach out
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