I believe topical lidocaine products are sold over-the-counter in most stores. It’s potentially another option, I suppose.
Anesthesiology. 2004 May;100(5):1206-10.
Lidocaine inhibits tyrosine kinase activity of the epidermal growth factor receptor and suppresses proliferation of corneal epithelial cells.
BACKGROUND: Although lidocaine is recognized as an excellent topical corneal analgesic, its toxic effect on corneal epithelial cells limits its use during corneal epithelial wound healing. Mechanism of the impairment of corneal reepithelialization with lidocaine, however, has not been evaluated. The authors’ previous study revealed that lidocaine inhibits the activity of tyrosine kinase receptors through the interaction with specific amino acid sequences around autophosphorylation sites, including acidic, basic, and aromatic amino acids. Epidermal growth factor receptor (EGFR), a tyrosine kinase receptor with an important role in epithelial cell proliferation after corneal wounding, also possesses these amino acids sequences around autophosphorylation sites. The authors hypothesized that lidocaine would suppress tyrosine kinase activity of EGFR and would impair corneal epithelial cell proliferation. METHODS: To investigate the effect of lidocaine (4 microM-40 mM) on epidermal growth factor (EGF)-stimulated autophosphorylation of EGFR, the authors studied purified EGFR in microtubes. They cultured human corneal epithelial cells (HCECs) with EGF and lidocaine to investigate the effect of lidocaine on cell proliferation and on autophosphorylation of EGFR in HCECs. RESULTS: Lidocaine (> or =400 microM) significantly suppressed EGF-stimulated autophosphorylation of the purified EGFR. In the HCEC study, EGF alone stimulated cell proliferation and increased autophosphorylation of EGFR in HCECs. Lidocaine (> or = 400 microM) significantly suppressed both the proliferation of HCECs promoted by EGF and EGF-stimulated autophosphorylation of EGFR. CONCLUSION: Lidocaine directly inhibits tyrosine kinase activity of EGFR and suppresses the corneal epithelial cell proliferation.
» I believe topical lidocaine products are sold over-the-counter in most
» stores. It’s potentially another option, I suppose.
»
» Anesthesiology. 2004 May;100(5):1206-10.
»
» Lidocaine inhibits tyrosine kinase activity of the epidermal growth
» factor receptor and suppresses proliferation of corneal epithelial
» cells.
»
» BACKGROUND: Although lidocaine is recognized as an excellent topical
» corneal analgesic, its toxic effect on corneal epithelial cells limits its
» use during corneal epithelial wound healing. Mechanism of the impairment of
» corneal reepithelialization with lidocaine, however, has not been
» evaluated. The authors’ previous study revealed that lidocaine inhibits the
» activity of tyrosine kinase receptors through the interaction with specific
» amino acid sequences around autophosphorylation sites, including acidic,
» basic, and aromatic amino acids. Epidermal growth factor receptor (EGFR), a
» tyrosine kinase receptor with an important role in epithelial cell
» proliferation after corneal wounding, also possesses these amino acids
» sequences around autophosphorylation sites. The authors hypothesized that
» lidocaine would suppress tyrosine kinase activity of EGFR and would impair
» corneal epithelial cell proliferation. METHODS: To investigate the effect
» of lidocaine (4 microM-40 mM) on epidermal growth factor (EGF)-stimulated
» autophosphorylation of EGFR, the authors studied purified EGFR in
» microtubes. They cultured human corneal epithelial cells (HCECs) with EGF
» and lidocaine to investigate the effect of lidocaine on cell proliferation
» and on autophosphorylation of EGFR in HCECs. RESULTS: Lidocaine (> or =400
» microM) significantly suppressed EGF-stimulated autophosphorylation of the
» purified EGFR. In the HCEC study, EGF alone stimulated cell proliferation
» and increased autophosphorylation of EGFR in HCECs. Lidocaine (> or = 400
» microM) significantly suppressed both the proliferation of HCECs promoted
» by EGF and EGF-stimulated autophosphorylation of EGFR. CONCLUSION:
» Lidocaine directly inhibits tyrosine kinase activity of EGFR and suppresses
» the corneal epithelial cell proliferation.
»
» PMID: 15114219 [PubMed - indexed for MEDLINE]
I wonder if the “toxic” effect on epilithial cells would have a negative effect if applied to the wound too soon before re-epilithialization? Any ideas? It would be fascinating to the nth degree if something sitting at the drug store could do what getfitinib would do for this process…
» Sounds like yet another thing to throw onto the big pile of “may be a
» beneficial topical, but we can’t guarantee that it won’t hurt the growth
» yet.”
Hmm… I used lidocaine on my scalp the same day as I did the wounding. Never thought of this to be messing with potential results. The problem is that I did pretty deep wounding with the sandpaper and without lidocaine it probably would have been pure hell, it did burn a lot afterward even with lidocaine.
I believe that deep wounding is crucial for it to work unfortunately. The examples in the patent are often punch holes or deep cuts, you dont see any example with a chemical peel, sunburn and so on.
There is also an informative picture on follicabio.com where they show how deep wounding is necessary, which I doubt could be done with chemicals. But people should still try the chemical peel so we know for sure if it works or not.
» Sounds like yet another thing to throw onto the big pile of “may be a
» beneficial topical, but we can’t guarantee that it won’t hurt the growth
» yet.”
Also I’d say its kinda important to get apropriate strength of EGRF inhibition. Its hard to tell how potent the lidocaine is
» There is also an informative picture on follicabio.com where they show how
» deep wounding is necessary, which I doubt could be done with chemicals. But
» people should still try the chemical peel so we know for sure if it works
» or not.
» » There is also an informative picture on follicabio.com where they show
» how
» » deep wounding is necessary, which I doubt could be done with chemicals.
» But
» » people should still try the chemical peel so we know for sure if it
» works
» » or not.
»
» can you post a link please?
I think he’s refering to this. It’s just a diagrammatical representation and cannot be taken as an accurate depth of wound penetration.
» I believe that deep wounding is crucial for it to work unfortunately. The
» examples in the patent are often punch holes or deep cuts, you dont see any
» example with a chemical peel, sunburn and so on.
They mention chemical peels in the patent as potential wounding candidates. While peels like AHAs and glycolic acid are probably not going to be strong enough (in my opinion), deep peeling agents like TCA and phenol can do a lot of damage. Depending on the concentration used, both agents can wipe out the epidermis, and start damaging the dermis. Phenol goes so deep that you have to get put under general anesthesia when having it done.
» I wonder if the “toxic” effect on epilithial cells would have a negative
» effect if applied to the wound too soon before re-epilithialization?
That’s the question that led me to this abstract. I was trying to figure out what effect inhibiting EGF might have on a fresh wound. I think it may have a negative effect, but I don’t know how negative, and whether it would ultimately have an effect on creating new follicles post-epithelialization.
Failing to wound deeply enough will probably go down as the biggest failure point in these home-brewed Folica experiments.
Small testing areas is one thing, but the whole top of the head is something else. I’m gonna pay a derm for “the big one” if we ever get this procedure nailed down & effective.
This whole process involves too much bullsh*t to be screwing around with getting it half right. Too much pain & time & money. It’s not exactly minox foam we’re dealing with anymore.
Paying a couple hundred bucks to a derm to get this done right under controlled conditions . . . it sure beats the bargain you get from FUE work.
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