There has been much controversial discussion lately about which substances target HDAC’s and which don’t. This argumentation was specifically related to antibiotics. I would like to use this thread to collect information regarding (any) substances that affect HDAC’s in a central place.
• cinoxacin (Cinobac) (Removed from clinical use)[110]
• flumequine (Flubactin) (genotoxic carcinogen)(veterinary use)
• nalidixic acid (NegGam, Wintomylon)[110] (genotoxic carcinogen)
• oxolinic acid (Uroxin) (currently unavailable in the United States)
• piromidic acid (Panacid) (currently unavailable in the United States)
• pipemidic acid (Dolcol) (currently unavailable in the United States)
• rosoxacin (Eradacil) (restricted use, currently unavailable in the United States)
Second-generation
The second-generation class is sometimes subdivided into “Class 1” and “Class 2”.[111]
• ciprofloxacin (Zoxan, Ciprobay, Cipro, Ciproxin)[110][112]
• enoxacin (Enroxil, Penetrex)[110] (removed from clinical use)
• fleroxacin (Megalone, Roquinol) (removed from clinical use)
• lomefloxacin (Maxaquin)[110](discontinued in the United States)
• nadifloxacin (Acuatim, Nadoxin, Nadixa) (currently unavailable in the United States)
• norfloxacin (Lexinor, Noroxin, Quinabic, Janacin)[110](restricted use)[113]
• ofloxacin (Floxin, Oxaldin, Tarivid)[110] (only as ophthalmic in the United States)
• pefloxacin (Peflacine) (currently unavailable in the United States)
• rufloxacin (Uroflox) (currently unavailable in the United States)
Third-generation
Unlike the first- and second-generations, the third-generation is active against streptococci.[111]
• balofloxacin (Baloxin) (currently unavailable in the United States)
• grepafloxacin (Raxar) (removed from clinical use)
• levofloxacin (Cravit, Levaquin)[110][112] Currently involved in MDL litigation in the United States due to unacceptable safety profile.[114]
• pazufloxacin (Pasil, Pazucross) (currently unavailable in the United States)
• sparfloxacin (Zagam)[110](currently unavailable in the United States),[115]
• temafloxacin (Omniflox) (removed from clinical use)[116]
• tosufloxacin (Ozex, Tosacin) (currently unavailable in the United States)
Fourth-generation
Fourth generation fluoroquinolones act at DNA gyrase and topoisomerase IV.[117] This dual action slows development of resistance.
• clinafloxacin[112](currently unavailable in the United States)
• gatifloxacin (Zigat, Tequin) (Zymar -opth.) (Tequin removed from clinical use)[118]
• gemifloxacin (Factive)
• moxifloxacin (Avelox,Vigamox)[110](restricted use).[119]
• sitafloxacin (Gracevit) (currently unavailable in the United States)
• trovafloxacin (Trovan) (removed from clinical use)[110][112]
• prulifloxacin (Quisnon) (currently unavailable in the United States)
Interesting. As you may have already read, JG crashed after using Dexamethasone as a provocation test. He had previously recovered from PFS (for three years) after having been on a brief course of Tamoxifen (anti-estrogen, anti-fungal): viewtopic.php?p=50972#p50972
Also, Awor, do you have any references/citations for Nystatin being an HDACI? I’d like to know why this is working for some of us. Thanks.
You are now providing evidence that SOME abx and antifungals have HDACi properties.
Which is NOT equivalent at all. This kind of logical fallacy is similar to a syllogism, but even worse. Like I already said, just because apples are fruit does NOT make it safe to conclude that all fruits are apples.
I have provided evidence that antibiotics streptomycin, gentamicin and penicillin cannot have significant HDACi properties.
I have also provided logical evidence that the azoles antifungals and nystatin (thus most likely also amphotericin B) cannot have significant HDACi properties.
Ive pointed to these argumentations many times and you never cared to adress them. I shoudlnt have to provide a link once again.
People have had result from nystatin and you got them convinced it was because of its alledged HDACi properties. Which I proved to be wrong.
Please provide proofs about NYSTATIN or AZOLES (or at least fluconazole) having HDACi properties or officially and publicly withdraw your claim. Recognizing a human mistake will help maintain some of your remaining credibility more than bogging yourself further down into more illogical or plain intellectually dishonest argumentation.
Also there already is a thread about HDAC targeting substance there viewtopic.php?f=27&t=6344&p=53706#p53706
It should be of the utmost interest to you as I posted a very well done and exhaustive table showing the nutritional epigenetics effects of various phytochemicals.
Also you shouldnt have had to paste such a lengthy wikipedia quote about quinolones having epigenetic effects. Their primary mode of action and target, like I said have always been bacterial DNA by design, thus their epigenetic effects not only comes as no suprise but are well expected. They also represent a specific and not THAT broadly used class of abx, unlike the length of the list you posted can lead to beleive. In most countries only cipro and levaquin are commonly used, usually (abusively) for UTIs and lower respiratory tract infections. For the record and some anecdoctal report, I have been exposed for 6 weeks to high doses of various of these antibiotics (levofloxacin, ciprofloxacin, moxifloxacin, and plurifloxacin… yes, ALL of these, sometimes in combiation, along with other non-quinolone abx) with NOTHING but deleterious effects.
I would expect nothing but deleterious effects by taking so much of any drug, esp these ones, and esp in combination.
But can you really dismiss these abx when taken in small doses for short periods of time? (As I have done for years now with success let alone no adverse effects). Just sayin.
No, one can’t dismiss, marginalize or celebrate these drugs without qualification. I think Venceremos is pointing out that they don’t have automatic magical HDACI-based life-giving healing properties. They can fight infection, they can also cause a lot of collateral damage. Big risk/reward ratio to consider. I know Venceremos is not against antibiotics, only their indiscriminate prescription by certain doctors who do not adequately disclose the risks, who prescribe in excessive doses, and who do not advise discontinuation upon the presentation of serious side effects/warnings. It doesn’t always take a long dose to experience these effects, though – I witnessed some guys get hit immediately, and I felt the effects of new drugs rapidly. They are no joke. I know that Flagyl (Metronidazole), a different class of antibiotic, helped you immensely, Visionquest, and I think that me, you, Venceremos, and many others are in agreement here that pathogens introduced via finasteride-induced immune weakness are a component of our illness that can’t be overlooked.
I cannot be so definitive, nothing has really been proved yet by our anecdotal individual successes with antiinfectious or immunomodulating substances, nor by a diagnosis of inflammatory pudendal neuropathy.
I cannot say “pathogen introduced” confidently and would add “overgrowth and/or morphogenesis of otherwise non-pathogenic elements of our natural flora” with the same lack of confidence.
So Id at least contrast the above sentence by saying something like “…via finasteride-induced disruptions of the immune system MAY BE a component of our illness, that can’t be overlooked.”
Also, thanks Xdog for clarifying my point that you understood perfectly (besides this minor but important nuance)
Sounds good. I want to get back to the bait and switch that Awor pulled on us above. He listed a million versions of the same drug with the same suffix (~75% of the listed drugs)…
But I see no mention of Nystatin or Azole-class antifungals, the stuff that is being broadly claimed to be HDAC inhibiting by association. Can anyone present any citations demonstrating that they are HDAC inhibiting? Thank you.