Lab Notes

Lab Notes

Compounds from tropical nut could help break nicotine, betel nut addictions

UF Health researchers have identified compounds derived from the areca palm nut that could help smokers and users of betel quid, a mix of areca palm nut that sometimes includes tobacco, break their addictions. Findings by Roger Papke, Ph.D., a professor in the UF College of Medicine’s department of pharmacology and therapeutics, and Nicole A. Horenstein, Ph.D., an associate professor in the department of chemistry, showed the nut’s active ingredient, arecoline, acts on the same receptor proteins in the brain as nicotine. The goal is to design a compound that targets only addiction-related receptors in the brain, meaning it could potentially treat nicotine and betel nut addictions without side effects. — Doug Bennett

UF researchers identify gene variant to personalize therapy for deadly form of leukemia

A genetic variation identified by UF Health researchers may help clinicians target acute myeloid leukemia, a rapidly spreading type of cancer that affects the bone marrow and blood. Researchers in the UF College of Pharmacy found genetic variation within patients with CD33 — a surface molecule that acts as a receptor for drug therapy on a leukemia cell — can predict the effectiveness of the anti-leukemic drug gemtuzumab ozogamicin, or GO. Cancer cells with adequate CD33 allow GO to bind and enter the cell, eventually killing it. Cells without CD33, or with altered CD33 due to genetic variation, will not respond to GO. — Matt Splett

Drug pair slows progression of muscular dystrophy in animal models

A pair of protein-inhibiting compounds is effective at slowing the progression of a form of muscular dystrophy in animal models, UF Health researchers have found. The compounds are intriguing for possible use by Duchenne muscular dystrophy patients because they can be taken orally, said David Hammers, Ph.D., a postdoctoral associate in the UF College of Medicine’s department of pharmacology and therapeutics. Two compounds, edasalonexent and CAT-1041, inhibited a protein that controls DNA transcription, drives inflammation and suppresses muscle stem cell regeneration. That protein, known as NF-kappaB, also inhibits muscle regeneration. The oral compounds have an advantage over intravenous treatments because they don’t cause an unwanted immune system response. — Doug Bennett