They could be on to something
I agree, it is a bit frustrating, and the UC Irvine group isn't even at the IND stage, they're still doing pre-clinical work. One company that is working on the same target is Bionomics. They still haven't even selected their drug candidate yet, although if you believe their material, they are due to pick their candidate any day now.
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gibbledygook
- Family Elder
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Genistein inhibits kv1.3 (give up milk and eat soy!).
<shortened url>
Red wine
<shortened url>
Zinc
<shortened url>
looks like green tea and curcumin inhibit potassium channels with different numbers...
<shortened url>
Red wine
<shortened url>
Zinc
<shortened url>
looks like green tea and curcumin inhibit potassium channels with different numbers...
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
Gibbledygook, thanks for the info. I'm always interested in excuses for drinking more red wine, and I already use soy milk...now to go read some of jimmylegs' rantings about zinc...
I also found this on Kv1.3
Minocycline decreases in vitro microglial motility, beta1-integrin, and Kv1.3 channel expression.
J Neurochem. 2007 Dec;103(5):2035-46. Epub 2007 Sep 14.
Nutile-McMenemy N, Elfenbein A, Deleo JA.
Department of Anesthesiology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA.
Minocycline is a semisynthetic, tetracycline derivative that exerts anti-inflammatory and neuroprotective effects unrelated to its anti-microbial action. We have previously shown that minocycline prevented peripheral nerve injury-induced mechanical allodynia. Minocycline's mechanisms of action as a neuroprotective and anti-allodynic agent are unknown.
In response to injury, microglia become activated, proliferate, and migrate. Resting microglia express voltage-dependent inward K(+) currents and blocking Kv1.3 channels has been shown to inhibit microglial-mediated neuronal death. We investigated the effect of minocycline on the expression of Kv channels, cell motility, and beta-integrin expression using primary rat cortical microglia, transwell assays, and by flow cytometry.
Minocycline significantly reduced microglial migration to cellular debris, astrocyte-conditioned medium, ADP, and algesic mediators and significantly reduced the expression of CD29 (beta(1)-integrin) but not CD18 (beta(2)-integrin). Minocycline reduced the effect of extracellular potassium and later decreased microglial Kv1.3 expression. In summary, we uncovered a novel effect of minocycline that demonstrates this agent decreases microglial beta(1)-integrin expression, which leads to inhibition of motility. We propose an in vivo model whereby reduced microglial trafficking to injured neurons following nerve injury decreases the release of proinflammatory mediators into the synaptic milieu, preventing neuronal sensitization, the pathological correlate to chronic pain.
Pubmed link
I also found this on Kv1.3
Minocycline decreases in vitro microglial motility, beta1-integrin, and Kv1.3 channel expression.
J Neurochem. 2007 Dec;103(5):2035-46. Epub 2007 Sep 14.
Nutile-McMenemy N, Elfenbein A, Deleo JA.
Department of Anesthesiology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA.
Minocycline is a semisynthetic, tetracycline derivative that exerts anti-inflammatory and neuroprotective effects unrelated to its anti-microbial action. We have previously shown that minocycline prevented peripheral nerve injury-induced mechanical allodynia. Minocycline's mechanisms of action as a neuroprotective and anti-allodynic agent are unknown.
In response to injury, microglia become activated, proliferate, and migrate. Resting microglia express voltage-dependent inward K(+) currents and blocking Kv1.3 channels has been shown to inhibit microglial-mediated neuronal death. We investigated the effect of minocycline on the expression of Kv channels, cell motility, and beta-integrin expression using primary rat cortical microglia, transwell assays, and by flow cytometry.
Minocycline significantly reduced microglial migration to cellular debris, astrocyte-conditioned medium, ADP, and algesic mediators and significantly reduced the expression of CD29 (beta(1)-integrin) but not CD18 (beta(2)-integrin). Minocycline reduced the effect of extracellular potassium and later decreased microglial Kv1.3 expression. In summary, we uncovered a novel effect of minocycline that demonstrates this agent decreases microglial beta(1)-integrin expression, which leads to inhibition of motility. We propose an in vivo model whereby reduced microglial trafficking to injured neurons following nerve injury decreases the release of proinflammatory mediators into the synaptic milieu, preventing neuronal sensitization, the pathological correlate to chronic pain.
Pubmed link