32 replies to this topic

[mikeinnaples]

I looked every where for Selepryl as that was my first choice, however every place I could find seems to be out of stock. With that said, I was going to settle with Cyprenil, but I became a little unnerved when I went to CytoPharms website ....yeah, granted they are a Mexican company, but the english and misspellings on the website are bad enough that it makes me question thier product.

Any thoughts on this product or any leads on Selepryl that is actually in stock?

[luv2increase]

I looked every where for Selepryl as that was my first choice, however every place I could find seems to be out of stock. With that said, I was going to settle with Cyprenil, but I became a little unnerved when I went to CytoPharms website ....yeah, granted they are a Mexican company, but the english and misspellings on the website are bad enough that it makes me question thier product.

Any thoughts on this product or any leads on Selepryl that is actually in stock?

I've been taking Cyprenil from cytopharmaonline.com for quite awhile. It is definitely legit!!!

[mikeinnaples]

Thanks.

[Ben]

I have some from amygdalin.co.uk (excellent seller by the by). It's legit.

[tpower]

I wouldn't use deprenyl mainly for its metabolism into amphetamine-related products. Keep in mind that some have financial reasons for promoting it...Just be wary.

[luv2increase]

I wouldn't use deprenyl mainly for its metabolism into amphetamine-related products. Keep in mind that some have financial reasons for promoting it...Just be wary.

haven't you seen the research that amphetamine in low amounts is actually good for the brain and cause plasticity? at 1mg daily for life-extension you will get .00000222222333 micrograms of amphetamine metabolites anyways. GEE

Edited by luv2increase, 15 August 2008 - 03:22 AM.

[tpower]

Can you back that value up luv2increase? According to this paper, http://dmd.aspetjour...t/full/25/6/657, "the metabolites excreted 2 days after administration of 2.5-10 mg of selegiline hydrochloride amounted to 44-58% of the dose." The paper also says that 37% of the metabolites end up as ®-Methamphetamine, and 3% end up as ®-Amphetamine. Do the math for yourself luv2increase. It's a far cry from the value that he gave out. .00000222222333 micrograms? Where the f' did that come from? The actual value is magnitudes higher! And for everyone else, please be cautious of luv2increase's advice on this topic. What he/she says is simply unscientific. Do you have a phD on selegiline? Or is it a business? =P

[luv2increase]

Here is a study for people afraid of the metabolite of methamphetamine from deprenyl:

Deprenyl treatment attenuates long-term pre- and post-synaptic changes evoked by chronic methamphetamine.
Davidson C, Chen Q, Zhang X, Xiong X, Lazarus C, Lee TH, Ellinwood EH.

Department of Psychiatry and Behavioral Sciences, Box 3870, Duke University Medical Center, Durham, NC 27710, USA. colda@duke.edu

Deprenyl, used clinically in Parkinson's disease, has multiple pharmacological effects which make it a good candidate to treat neurotoxicity. Thus, we investigated deprenyl's ability to attenuate methamphetamine-induced dopamine neurotoxicity. We also examined deprenyl's effect in changing markers associated with psychostimulant sensitization. A potential therapeutic effect on either pathological domain would be a boon in developing novel treatments for methamphetamine abuse. Adult male Sprague-Dawley rats were split into 6 groups. Three groups received a 7-day saline minipump with saline, 0.05 or 0.25 mg/kg SC deprenyl injections given for 10 days before, during and 5 days after the 7-day saline minipump implant. Similarly, 3 groups received methamphetamine pumps (25 mg/kg/day) with escalating daily injections of methamphetamine (0-6 mg/kg) in addition to the minipump treatment. These rats also received saline, 0.05 or 0.25 mg/kg deprenyl injections given before, during and the 7-day minipump treatment. Rats were killed on day 28 of withdrawal and brain samples taken. HPLC analysis for dopamine and 3,4-Dihydroxy-Phenylacetic Acid (DOPAC) revealed a loss of dopamine in the caudate and accumbens which was partially reversed by high dose deprenyl. Tyrosine hydroxylase immunostaining in the midbrain was unaffected by methamphetamine, suggesting that dopamine neurotoxicity was localized to the caudate. Western blot analysis of the caudate after methamphetamine revealed little change in Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid (AMPA) GluR1 or N-Methyl-d-Aspartate (NMDA) NR2B subunits, or their phosphorylation state. However, methamphetamine increased levels of GluR1 and its phosphorylation state in the prefrontal cortex (PFC), and these increases were attenuated by deprenyl. Methamphetamine also increased levels of PFC NR2B subunit, but these increases were not attenuated by deprenyl. We suggest that deprenyl may be effective in reducing the neurotoxic effects of methamphetamine and may also attenuate changes in prefrontal AMPA receptor function, presumably more associated with addiction rather than neurotoxicity.

This study has been brought up before here Imminst, and I can't believe I had forgotten to mention it. Even though methamphetamine is a metabolite, it seems as though selegiline actually attenuates the negative affects from it. This is very important.

Also, Desoxyn is a pure pharmaceutical grade medication of methamphetamine used successfully to treat AD/HD. This is very important because in therapeutic dosages, methamphetamine is not shown to be negative at all. It is only when Meth Addicts consume non-therapeutic mega doses for extreme periods of time does it really mess someone up in a very bad way. Compare the low dose of selegiline metabolites of methamphetamine to the massive (multiple grams throughout many days) doses that the drug addicts consume.

You have to get the stigma out of your head of automatically considering methamphetamine bad, especially when it comes to extremely low dosages.


Selegiline is a win-win!

End of argument....

[mikeinnaples]

Is they person just posting the same crap in every deprenyl thread?

[tpower]

Here is a study for people afraid of the metabolite of methamphetamine from deprenyl:

Deprenyl treatment attenuates long-term pre- and post-synaptic changes evoked by chronic methamphetamine.
Davidson C, Chen Q, Zhang X, Xiong X, Lazarus C, Lee TH, Ellinwood EH.

Department of Psychiatry and Behavioral Sciences, Box 3870, Duke University Medical Center, Durham, NC 27710, USA. colda@duke.edu

Deprenyl, used clinically in Parkinson's disease, has multiple pharmacological effects which make it a good candidate to treat neurotoxicity. Thus, we investigated deprenyl's ability to attenuate methamphetamine-induced dopamine neurotoxicity. We also examined deprenyl's effect in changing markers associated with psychostimulant sensitization. A potential therapeutic effect on either pathological domain would be a boon in developing novel treatments for methamphetamine abuse. Adult male Sprague-Dawley rats were split into 6 groups. Three groups received a 7-day saline minipump with saline, 0.05 or 0.25 mg/kg SC deprenyl injections given for 10 days before, during and 5 days after the 7-day saline minipump implant. Similarly, 3 groups received methamphetamine pumps (25 mg/kg/day) with escalating daily injections of methamphetamine (0-6 mg/kg) in addition to the minipump treatment. These rats also received saline, 0.05 or 0.25 mg/kg deprenyl injections given before, during and the 7-day minipump treatment. Rats were killed on day 28 of withdrawal and brain samples taken. HPLC analysis for dopamine and 3,4-Dihydroxy-Phenylacetic Acid (DOPAC) revealed a loss of dopamine in the caudate and accumbens which was partially reversed by high dose deprenyl. Tyrosine hydroxylase immunostaining in the midbrain was unaffected by methamphetamine, suggesting that dopamine neurotoxicity was localized to the caudate. Western blot analysis of the caudate after methamphetamine revealed little change in Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid (AMPA) GluR1 or N-Methyl-d-Aspartate (NMDA) NR2B subunits, or their phosphorylation state. However, methamphetamine increased levels of GluR1 and its phosphorylation state in the prefrontal cortex (PFC), and these increases were attenuated by deprenyl. Methamphetamine also increased levels of PFC NR2B subunit, but these increases were not attenuated by deprenyl. We suggest that deprenyl may be effective in reducing the neurotoxic effects of methamphetamine and may also attenuate changes in prefrontal AMPA receptor function, presumably more associated with addiction rather than neurotoxicity.

This study has been brought up before here Imminst, and I can't believe I had forgotten to mention it. Even though methamphetamine is a metabolite, it seems as though selegiline actually attenuates the negative affects from it. This is very important.

Also, Desoxyn is a pure pharmaceutical grade medication of methamphetamine used successfully to treat AD/HD. This is very important because in therapeutic dosages, methamphetamine is not shown to be negative at all. It is only when Meth Addicts consume non-therapeutic mega doses for extreme periods of time does it really mess someone up in a very bad way. Compare the low dose of selegiline metabolites of methamphetamine to the massive (multiple grams throughout many days) doses that the drug addicts consume.

You have to get the stigma out of your head of automatically considering methamphetamine bad, especially when it comes to extremely low dosages.


Selegiline is a win-win!

End of argument....

I think you're over-simplifying things here luv2increase. First of all, attentuation is not equivalent to reversion in biochemistry. If something is toxic, then it is. DNA gets damaged. End of story. Whether you can partially attenuate the effects of the chemicals is a whole different matter; as stated in the paper's abstract, selegiline in its pure form, seems to be able to partially preserve some of the changes made by its metabolites. This does not in anyway indicate that selegiline is able to avoid cellular DNA damage caused by its metabolites, which would be miraculous if it did. It might be able to upregulate a particular protein that its metabolites downregulated, but the damage has been done. The DNA is no longer as good as it was.

Also, when you ingest chemicals into your body, for the most part, you would want to know if any cells in your body are being damaged at all. The studies done on selegiline were mostly done on its effects on the brain. Most genotoxic chemicals will damage the dna of all cells, not just of neurons. I would definitely be extra cautious knowing that amphetamine-related chemicals are known to be toxic to cells. For instance, cardiovascular toxicity has been reported with the use of selegiline in people with Parkinson's. I wouldn't be surprised if you could extrapolate that data to normal people.

Furthermore, having gone through the literature on selegiline, I personally do not see any papers on selegiline citrate. To me it appears to be a scam. The studies I've seen were done with selegiline HCL. I would not be so enthusiastic about a chemical (selegiline citrate) with very little evidence supporting its existence, AS WELL AS its efficacy over selegiline HCL. It's incomprehensive to me how someone who claims that he/she is scientifically sound can be so ebullient over selegiline. I would avoid it at all costs. Around 40 to 50% of the selegiline gets metabolised in the liver, a significant amount. If you try avoiding the first-pass metabolism, you risk oral toxicity, and hence, oral cancers.

Know that you have been forewarned. Selegiline is not a win-win in my book. I would also not trust the advice of someone (luv2increase) who makes up a number out of the blue just to support his argument that selegiline is "good." Selegiline is a risky compound to use, even at low dose levels. Biochemistry is complex; an extreme reductionist attitude is not conducive to scientific inquiry.

Out.

Edit: an ambiguous word.

Edited by tpower, 15 August 2008 - 07:32 PM.

[luv2increase]

Here is a study for people afraid of the metabolite of methamphetamine from deprenyl:

Deprenyl treatment attenuates long-term pre- and post-synaptic changes evoked by chronic methamphetamine.
Davidson C, Chen Q, Zhang X, Xiong X, Lazarus C, Lee TH, Ellinwood EH.

Department of Psychiatry and Behavioral Sciences, Box 3870, Duke University Medical Center, Durham, NC 27710, USA. colda@duke.edu

Deprenyl, used clinically in Parkinson's disease, has multiple pharmacological effects which make it a good candidate to treat neurotoxicity. Thus, we investigated deprenyl's ability to attenuate methamphetamine-induced dopamine neurotoxicity. We also examined deprenyl's effect in changing markers associated with psychostimulant sensitization. A potential therapeutic effect on either pathological domain would be a boon in developing novel treatments for methamphetamine abuse. Adult male Sprague-Dawley rats were split into 6 groups. Three groups received a 7-day saline minipump with saline, 0.05 or 0.25 mg/kg SC deprenyl injections given for 10 days before, during and 5 days after the 7-day saline minipump implant. Similarly, 3 groups received methamphetamine pumps (25 mg/kg/day) with escalating daily injections of methamphetamine (0-6 mg/kg) in addition to the minipump treatment. These rats also received saline, 0.05 or 0.25 mg/kg deprenyl injections given before, during and the 7-day minipump treatment. Rats were killed on day 28 of withdrawal and brain samples taken. HPLC analysis for dopamine and 3,4-Dihydroxy-Phenylacetic Acid (DOPAC) revealed a loss of dopamine in the caudate and accumbens which was partially reversed by high dose deprenyl. Tyrosine hydroxylase immunostaining in the midbrain was unaffected by methamphetamine, suggesting that dopamine neurotoxicity was localized to the caudate. Western blot analysis of the caudate after methamphetamine revealed little change in Alpha-Amino-3-Hydroxy-5-Methyl-4-Isoxazole Propionic Acid (AMPA) GluR1 or N-Methyl-d-Aspartate (NMDA) NR2B subunits, or their phosphorylation state. However, methamphetamine increased levels of GluR1 and its phosphorylation state in the prefrontal cortex (PFC), and these increases were attenuated by deprenyl. Methamphetamine also increased levels of PFC NR2B subunit, but these increases were not attenuated by deprenyl. We suggest that deprenyl may be effective in reducing the neurotoxic effects of methamphetamine and may also attenuate changes in prefrontal AMPA receptor function, presumably more associated with addiction rather than neurotoxicity.

This study has been brought up before here Imminst, and I can't believe I had forgotten to mention it. Even though methamphetamine is a metabolite, it seems as though selegiline actually attenuates the negative affects from it. This is very important.

Also, Desoxyn is a pure pharmaceutical grade medication of methamphetamine used successfully to treat AD/HD. This is very important because in therapeutic dosages, methamphetamine is not shown to be negative at all. It is only when Meth Addicts consume non-therapeutic mega doses for extreme periods of time does it really mess someone up in a very bad way. Compare the low dose of selegiline metabolites of methamphetamine to the massive (multiple grams throughout many days) doses that the drug addicts consume.

You have to get the stigma out of your head of automatically considering methamphetamine bad, especially when it comes to extremely low dosages.


Selegiline is a win-win!

End of argument....

I think you're over-simplifying things here luv2increase. First of all, attentuation is not equivalent to reversion in biochemistry. If something is toxic, then it is. DNA gets damaged. End of story. Whether you can partially attenuate the effects of the chemicals is a whole different matter; as stated in the paper's abstract, selegiline in its pure form, seems to be able to partially preserve some of the changes made by its metabolites. This does not in anyway indicate that selegiline is able to avoid cellular DNA damage caused by its metabolites, which would be miraculous if it did. It might be able to upregulate a particular protein that its metabolites downregulated, but the damage has been done. The DNA is no longer as good as it was.

Also, when you ingest chemicals into your body, for the most part, you would want to know if any cells in your body are being damaged at all. The studies done on selegiline were mostly done on its effects on the brain. Most genotoxic chemicals will damage the dna of all cells, not just of neurons. I would definitely be extra cautious knowing that amphetamine-related chemicals are known to be toxic to cells. For instance, cardiovascular toxicity has been reported with the use of selegiline in people with Parkinson's. I wouldn't be surprised if you could extrapolate that data to normal people.

Furthermore, having gone through the literature on selegiline, I personally do not see any papers on selegiline citrate. To me it appears to be a scam. The studies I've seen were done with selegiline HCL. I would not be so enthusiastic about a chemical (selegiline citrate) with very little evidence supporting its existence, AS WELL AS its efficacy over selegiline HCL. It's incomprehensive to me how someone who claims that he/she is scientifically sound can be so ebullient over selegiline. I would avoid it at all costs. Around 40 to 50% of the selegiline gets metabolised in the liver, a significant amount. If you try avoiding the first-pass metabolism, you risk oral toxicity, and hence, oral cancers.

Know that you have been forewarned. Selegiline is not a win-win in my book. I would also not trust the advice of someone (luv2increase) who makes up a number out of the blue just to support his argument that selegiline is "good." Selegiline is a risky compound to use, even at low dose levels. Biochemistry is complex; an extreme reductionist attitude is not conducive to scientific inquiry.

Out.

Edit: an ambiguous word.

I think you are getting L-Methamphetamine and D-Methamphetamine confused bro.

You are trying to correlate d-amphetamine to selegiline which is just plain awful.

Instead of listening to me or tpower, I think all need to be done for you people to go to google scholar and search for selegiline. All the positive info will be there. I can't seem to find any negative study whatsoever on deprenyl or its metabolites yet quite the contrary.


Tpower, show me some negative studies on deprenyl, selegiline (whichever) and post it on this thread. Back up your talk please.

I HAVEN'T SEEN ONE SCIENTIFIC STUDY POSTED FROM YOU EXCEPT FOR THAT SELEGILINE IS METABOLIZED IN THE LIVER TO "L-METHAMPHETAMINE". You have to do better than that. That doesn't prove anything considering the amount is so small and it is once again the L version and not the D (toxic) version.


edit: mouth cancer??? show me a study to back that one up also

also would like to add that I am not a proponent of oral deprenyl yet only selegiline citrate which is just like trandermal IMO that it lacks the formation of l-methamphetamine etc.. metabolites as found in this dog study --->

oxicokinetic evaluation of a selegiline transdermal system in the dog.
Barrett JS, DiSanto AR, Thomford PJ, Larsen EM, Palazzolo MJ, Morales RJ.

Somerset Pharmaceuticals, Tampa, FL, USA. jsb@somersetpharm.com

The toxicology and toxicokinetics of a selegiline transdermal system (STS) were evaluated in a 3 month dog study of daily 24 h applications of placebo 4, 8, or 12 STSs in 32 male and 32 female beagle dogs. Each STS delivered approximately 5 mg selegiline over 24 h. No drug-related signs of toxicity were noted in any group with respect to clinical observations, dermal effects, body weight, food consumption, hematology, urinalysis data, or ophthalmoscopic or electrocardiographic examinations. Clinical chemistry data revealed no consistent adverse effects except for an increase in alanine aminotransferase in dogs receiving 8 and 12 STSs. Histological evaluation of tissues revealed the presence of pigment in the Kupffer cells of dogs treated with 8 and 12 STSs. There were no pathology findings suggestive of hemolysis or cholestasis. The no-effect level (NOEL) was 4 STSs (2.9 mg kg-1 d-1). There were no degenerative or life-threatening toxic effects up to 12 STSs (8.5 mg kg-1 d-1). Gender-related differences in steady-state plasma levels were not observed. Steady-state plasma concentrations were similar to maximum plasma concentrations obtained in single-dose studies, suggesting that drug accumulation was not evident. Simulation of systemic exposure following oral administration of 16.8 mg kg-1 d-1 from previous toxicology studies indicated that selegiline exposure following 12 STSs is sixfold greater while N-desmethylselegiline, L-amphetamine, and L-methamphetamine exposure is 0.5, 0.15, and 0.14 times the exposure in the oral study. The threefold difference in NOEL between oral and transdermal studies in the dog (0.8 versus 2.9 mg kg-1 d-1) is probably related to greater L-amphetamine and L-methamphetamine exposure following oral administration. The reduction in metabolite formation, relative exposure of selegiline in the dog at the NOEL compared to oral toxicology studies, and margin of safety provided, given that the expected clinical dose is less than the dosage of oral Eldepryl (0.15 mg kg-1 d-1), documents the safety of the selegiline drug substance and indicates that additional toxicologic findings with the STS may not be expected.

PMID: 9099452 [PubMed - indexed for MEDLINE]

Edited by luv2increase, 15 August 2008 - 09:51 PM.

[Advanc3d]

just a question kinda off topic


luv2increase, since i dont have selegiline citrate, would you say taking Selegiline HCL 2.5mg under the tongue is better than orally ingesting it?
how much is the bioavailabity increased compared to oral?

[luv2increase]

just a question kinda off topic


luv2increase, since i dont have selegiline citrate, would you say taking Selegiline HCL 2.5mg under the tongue is better than orally ingesting it?
how much is the bioavailabity increased compared to oral?

There is a selegiline hcl prescription on the market now called Zelapar. I would assume it would work well. It may take a while to to dissolve so you may want to crush it up and place powder under tongue.

I think you'd be best to just get the liquid selegiline citrate next time around.

Also, remember that the citrate and hydrochloride are just the carriers for the base (selegiline). I would think that the hcl under the tongue would work just as well as the citrate POSSIBLY. I do know that the majority of anecdotal reports on the net report that orally taking selegiline hcl (l-deprenyl) gives more of a speedy feeling with unwanted side-effects. This may be due to the fact of the metabolites which it produces???



Finish up what you have and get the liquid next time. Also, make note on your experiences on trying the selegiline hcl under the tongue and compare it to the liquid citrate when you experience it. It would be interesting to know.


Good Luck!

[bgwithadd]

If anything, methamphetamine is going to be safer than amphetamine. The reason is that it's more powerful and you are therefore using far smaller effective doses. Desoxyn works well for this reason. Unfortunately there's no longer any long acting desoxyn, and in my mind insant release stims are pretty questionable as ADD treatments. Yes they can work but are easy to abuse. I was not aware of deprynyl before, and what especially looks interesting is the emsam patch. 15 hours would be absolutely perfect, if it works at all. I may try to get this.

Also, talking about toxicity in high doses is pretty ridiculous, because virtually anything is neurotoxic at high enough doses, but the concentration level is what matters. No one will prescribe you something in neurotoxic doses, end of story, so there is no point in bringing it up unless you are talking about drug abuse instead of drug therapy.

[luv2increase]

15 hours would be absolutely perfect, if it works at all. I may try to get this.

I want to make sure you know that selegiline is an irreversible MAO-B inhibitor. Due to this, the effects from the drug will last possibly up to two weeks in your system. This is also cumulative, in that you may not achieve MAO-B inhibition with daily 1-2mg doses but after 2-3 weeks or more, it will eventually happen. At this point, you may want to take a break.

Better yet, if you are young and are looking at soley life-extension, 1mg every other day to every 3 days should suffice.

[bgwithadd]

Hmm, I was excited about it at first as an ADD/depression cure, but I am guessing the doses needed for that might require diet restrictions. A 15 hour patch for amphetamine or methamphetamine at low, therapeutic doses would be perfect for me, though.

[Advanc3d]

just a question kinda off topic


luv2increase, since i dont have selegiline citrate, would you say taking Selegiline HCL 2.5mg under the tongue is better than orally ingesting it?
how much is the bioavailabity increased compared to oral?

There is a selegiline hcl prescription on the market now called Zelapar. I would assume it would work well. It may take a while to to dissolve so you may want to crush it up and place powder under tongue.

I think you'd be best to just get the liquid selegiline citrate next time around.

Also, remember that the citrate and hydrochloride are just the carriers for the base (selegiline). I would think that the hcl under the tongue would work just as well as the citrate POSSIBLY. I do know that the majority of anecdotal reports on the net report that orally taking selegiline hcl (l-deprenyl) gives more of a speedy feeling with unwanted side-effects. This may be due to the fact of the metabolites which it produces???



Finish up what you have and get the liquid next time. Also, make note on your experiences on trying the selegiline hcl under the tongue and compare it to the liquid citrate when you experience it. It would be interesting to know.


Good Luck!

the eldepryl selegiline HCL dissolves and disapears within like 1 minute when the whole tablet is placed under my tongue.
after 5min theres virtually nothing in my mouth other than saliva. then i wash it down after 10min.

is there a method to turn ordinary Selegiline tablet HCL in to a transdermal patch?

Edited by Advanc3d, 19 August 2008 - 12:46 AM.

[graatch]

If anything, methamphetamine is going to be safer than amphetamine. The reason is that it's more powerful and you are therefore using far smaller effective doses.

This is quite true -- methamphetamine is more central.

I am personally concerned about an additional mechanism of neurotoxicity with methamphetamine (affinity for serotonergic release) that I think, unlike with dextroamphetamine (for which this is not relevant at all at therapeutic doses), may be active within typical therapeutic dosing ranges.

Frangible tells me that serotonergic affinity is still very slim at these doses, though, and he has researched this in more depth than me.

Hmm, I was excited about it at first as an ADD/depression cure, but I am guessing the doses needed for that might require diet restrictions.

The FDA requires dietary restrictions for all but the smallest EMSAM patch, but a good deal of evidence and a vagary of selegiline's interaction with tyramine suggests that diet restrictions are not much of an issue with these patches either, despite full inhibition of MAO-A. Taking stimulants with it, however, is still dangerous and requires extreme care, best done with the help of a doctor.

A 15 hour patch for amphetamine or methamphetamine at low, therapeutic doses would be perfect for me, though.

The methylphenidate patch, while overall ineffective for me, I found to last at least 16 hours with no drop in effect. There is enough methylphenidate to continue a steady release past the 9 hours (and past the 12 hours the company sought FDA approval for.) This is the experience in some anecdotal reports too, though not all. Some people leave the patch on at night, finding it to improve their sleep.

Shire is researching an amphetamine patch, but this will probably not see the light of day for the duration of two or three patents, eh?

[tpower]

The paper that talks about the oral toxicity is titled "Sublingual selegiline (new formulation) Oral toxicity further compounds already unfavourable risk-benefit ratio." It is published in 2003 in the journal PRESCRIRE INTERNATIONAL. Also, L enantiomers of amphetamines ARE toxic. Stop brainwashing people into believing that they're not. Both are.

luv2increase, you seem to encourage the use of liquid selegiline (aka. cytopharma's hotseller, selegiline citrate, whatever that is) everywhere.

Please defend its use.

Also, to the other guy who posted here, doctors pescribe toxic pharmaceuticals ALL THE TIME. That's why there is an academic discipline called toxicology for crying out loud! Downplaying the toxicity risks of selegiline is not smart to do. Especially in light of a paper that says that about 40 to 50% of oral selegiline gets metabolised into other products, and 37% of them become L enantiomers of amphetamines.

Wake up!

[tpower]

Also luv2increase, please explain why liquid selegiline would NOT get metabolized. It think it is disingenuous to assert something as bold as that when science runs against that bold statement. In short, the liver doesn't give a damn whether or not selegiline is in liquid form; it also doesn't give a damn which ion binds to the selegiline. When the salt gets dissolved in the gut, the ions separate and the liver has to metabolise the selegiline regardless.

[luv2increase]

The paper that talks about the oral toxicity is titled "Sublingual selegiline (new formulation) Oral toxicity further compounds already unfavourable risk-benefit ratio." It is published in 2003 in the journal PRESCRIRE INTERNATIONAL. Also, L enantiomers of amphetamines ARE toxic. Stop brainwashing people into believing that they're not. Both are.

luv2increase, you seem to encourage the use of liquid selegiline (aka. cytopharma's hotseller, selegiline citrate, whatever that is) everywhere.

Please defend its use.

Also, to the other guy who posted here, doctors pescribe toxic pharmaceuticals ALL THE TIME. That's why there is an academic discipline called toxicology for crying out loud! Downplaying the toxicity risks of selegiline is not smart to do. Especially in light of a paper that says that about 40 to 50% of oral selegiline gets metabolised into other products, and 37% of them become L enantiomers of amphetamines.

Wake up!

I bid you to take a LONG gander at the other thread and to atleast refrain from posting in the other thread any more unless it deals with 'DRUG TESTS'.

Will you quit posting hypothetical beliefs and post real scientific evidence. It is getting old. You won't get too far on here with your theories.

[tpower]

I have posed a valid point. Read the article on sublingual selegiline being orally toxic. I have also posed a valid point in warning people about the percentage of metabolites created by the liver via the oral route. If the buccal administration bypasses liver metabolism, that is great. However, oral toxicity is still a real threat, and the buccal route for many drugs only reduce metabolite creation by around 90%.

I pose a question to all of you; what do I have to gain by telling you all to be wary of administering selegiline? Only sellers have much to gain.

I think your presuming that I have given out pseudo-scientific knowledge borders on arrogance. The reality is that it is you who has espoused pseudo-intelligence by abusing the number of posts you have made and misdirecting people into blindly believing that something they are taking is safe. If you really believed in science, you would have at least taken some time to consider the issue of oral toxicity of sublingual forms of selegiline. Unfortunately, you have not. From this I have to conclude that you do not adopt a scientific attitude to viewing things.

You also seem to demoralize people for raising viewpoints supported by scientific papers. Perhaps you should refrain from rejecting scientific facts and take a hard look at the evidence that I've given. That is what I call a good scientific approach.

[luv2increase]

I have posed a valid point. Read the article on sublingual selegiline being orally toxic. I have also posed a valid point in warning people about the percentage of metabolites created by the liver via the oral route. If the buccal administration bypasses liver metabolism, that is great. However, oral toxicity is still a real threat, and the buccal route for many drugs only reduce metabolite creation by around 90%.

I pose a question to all of you; what do I have to gain by telling you all to be wary of administering selegiline? Only sellers have much to gain.

I think your presuming that I have given out pseudo-scientific knowledge borders on arrogance. The reality is that it is you who has espoused pseudo-intelligence by abusing the number of posts you have made and misdirecting people into blindly believing that something they are taking is safe. If you really believed in science, you would have at least taken some time to consider the issue of oral toxicity of sublingual forms of selegiline. Unfortunately, you have not. From this I have to conclude that you do not adopt a scientific attitude to viewing things.

You also seem to demoralize people for raising viewpoints supported by scientific papers. Perhaps you should refrain from rejecting scientific facts and take a hard look at the evidence that I've given. That is what I call a good scientific approach.

Where is your post about selegiline being toxic in the mouth? I can't seem to find it. I can't find it on pubmed either.

I am going to get a little ad-hominem for a second also real quick. I think you being diagnosed as a hypochondriac leads you to be petrified of just about everything to a larger extent than normal people. This has been evidenced by the way you post. Do you realize that literally almost 100% of everything you intake in your body has toxins in it, and wants it gets in your body creates more toxins? Quit being so scared or go build your self a bubble and starve to death. j/k


Back on topic. Post the study on the toxicity of selegiline in the oral cavity again, thanks!!!

[brotherx]

Hi tpower,

could you post the study?

Cheers

Alex

I have posed a valid point. Read the article on sublingual selegiline being orally toxic. I have also posed a valid point in warning people about the percentage of metabolites created by the liver via the oral route. If the buccal administration bypasses liver metabolism, that is great. However, oral toxicity is still a real threat, and the buccal route for many drugs only reduce metabolite creation by around 90%.

I pose a question to all of you; what do I have to gain by telling you all to be wary of administering selegiline? Only sellers have much to gain.

I think your presuming that I have given out pseudo-scientific knowledge borders on arrogance. The reality is that it is you who has espoused pseudo-intelligence by abusing the number of posts you have made and misdirecting people into blindly believing that something they are taking is safe. If you really believed in science, you would have at least taken some time to consider the issue of oral toxicity of sublingual forms of selegiline. Unfortunately, you have not. From this I have to conclude that you do not adopt a scientific attitude to viewing things.

You also seem to demoralize people for raising viewpoints supported by scientific papers. Perhaps you should refrain from rejecting scientific facts and take a hard look at the evidence that I've given. That is what I call a good scientific approach.

[brotherx]

In the patent for "US Patent 6117912 - Sublingual and buccal administration of selegiline for treating certain selegiline-responsive diseases and conditions" it is stated that

"The present invention is based upon the discovery that certain diseases and
conditions for which selegiline is known to be useful are surprisingly and
unexpectedly more advantageously treated by administering selegiline
buccally or sublingually rather than by administering selegiline using
prior art methods, e.g., oral administration. Accordingly, the novel
methods disclosed herein produce enhanced therapeutic effects."

Here is no hint regarding oral toxicity. On the website of the world intellectual property organization you find the following statement:

"Selegiline provides neuroprotection or neuronal rescue, by one or more mechanisms, for example, by reducing oxidative neuronal damage, increasing the amount of the enzyme superoxide dismutase, and/or reducing dopamine catabolism. PCT Published Application WO 92/17169 discloses that selegiline acts by directly maintaining, preventing loss of, and/or assisting in, the nerve function of animals. [...]" ((WO/1997/017067) SUBLINGUAL AND BUCCAL ADMINISTRATION OF SELEGILINE"

There is an article: "Sublingual selegiline (new formulation) Oral toxicity further compounds already unfavourable risk-benefit ratio". I haven't checked yet if I can use my world wide library access to read that article for free.
But you can try yourself - it can be found here: http://direct.bl.uk/...om=searchengine

Now switching to another interesting topic - how to prepare a selegiline to be more bioavailable:

Have a look on the "Sublingual Selegiline Tablet (Effervescent)" example below.
There you find that the additional key ingredients are: Citric Acid & Fumaric Acid. Those 2 substances seem to improve biovailability a great deal (Somewhere I have that study about Effervescent).


"DETAILED DESCRIPTION OF THE INVENTION

EXAMPLE 1

Buccal Selegiline Tablet

A buccal tablet is formulated from the following ingredients:


______________________________________
Ingredient Weight (mg/unit dose)
______________________________________
Selegiline HCl 5.00
Hydroxypropylmethlycellulose (HPMC) 5.00
Lactose 186.00
Citric Acid (anhydrous) 2.00
Magnesium stearate 2.00
______________________________________



Prepare a granulate from the first four ingredients by first passing
ingredients 1, 3 and 4 though a 25-mesh hand screen and thereafter blend.
Prepare a 10% solution of HPMC in water (10 g HPMC per 100 g of solution)
and granulate this solution into the dry ingredients. Pass the wet mass
through a #10 screen and spread onto a paper-lined tray, drying for three
hours at 130° C. Blend the resulting granulate with ingredient 5
and compress into a tablets.

EXAMPLE 2

Sublingual Selegiline Tablet (Non-Effervescent)

A sublingual tablet is prepared from the following ingredients:


______________________________________
Ingredient Weight (mg/unit dose)
______________________________________
Selegiline HCl 5.00
Croacarmellose sodium 5.00
Lactose 186.00
Citric Acid (anhydrous) 2.00
Magnesium stearate 2.00
______________________________________



Pass the first three ingredients above through a 25-mesh hand screen and
blend and mix for seven minutes. After passing ingredient 4 above through
a #60 hand mesh, add to the mix with the remaining blended ingredients and
blend for an additional 3 minutes. Compress the resulting mixture into
tablets.

EXAMPLE 3

Sublingual Selegiline Tablet (Effervescent)

A sublingual tablet is prepared from the following ingredients:


______________________________________
Ingredient Weight (mg/unit dose)
______________________________________
Selegiline HCl 5.00
Citric Acid (anhydrous) 100.00
Sodium bicarbonate 185.00
Fumaric acid 10.00"
______________________________________




Sources:
http://www.patentsto...escription.html
http://www.wipo.int/...mp;DISPLAY=DESC
http://direct.bl.uk/...om=searchengine



Cheers Alex




--------------------

I have posed a valid point. Read the article on sublingual selegiline being orally toxic. I have also posed a valid point in warning people about the percentage of metabolites created by the liver via the oral route. If the buccal administration bypasses liver metabolism, that is great. However, oral toxicity is still a real threat, and the buccal route for many drugs only reduce metabolite creation by around 90%.

I pose a question to all of you; what do I have to gain by telling you all to be wary of administering selegiline? Only sellers have much to gain.

I think your presuming that I have given out pseudo-scientific knowledge borders on arrogance. The reality is that it is you who has espoused pseudo-intelligence by abusing the number of posts you have made and misdirecting people into blindly believing that something they are taking is safe. If you really believed in science, you would have at least taken some time to consider the issue of oral toxicity of sublingual forms of selegiline. Unfortunately, you have not. From this I have to conclude that you do not adopt a scientific attitude to viewing things.

You also seem to demoralize people for raising viewpoints supported by scientific papers. Perhaps you should refrain from rejecting scientific facts and take a hard look at the evidence that I've given. That is what I call a good scientific approach.

Edited by brotherx, 20 August 2008 - 10:05 AM.

[tpower]

In retrospect, I might have been too risk-adverse in my attitude towards selegiline. My intent was to highlight potential factors that might influence people's choice of drugs/supplements. I also wish to emphasize that I had no interest in maligning luv2increase; he/she is an invaluable poster to this forum, and if I came off as too big of an asshole towards him, then I give my apologies.

[luv2increase]

In retrospect, I might have been too risk-adverse in my attitude towards selegiline. My intent was to highlight potential factors that might influence people's choice of drugs/supplements. I also wish to emphasize that I had no interest in maligning luv2increase; he/she is an invaluable poster to this forum, and if I came off as too big of an asshole towards him, then I give my apologies.

Apology accepted! I would also like to offer an apology to you as well.

[mikeinnaples]

Ok ....update.

I receive my Cyprenil on Saturday and have been taking 1-2mg every other day. It is definately doing something.

For example, I had been feeling overstimulated from Racetams and Choline, but adding the Cyprenil seemed to help me get a handle on it and my focus has increased. Placebo effect possibly .....we shall see, but so far I am happy with it.

[luv2increase]

Ok ....update.

I receive my Cyprenil on Saturday and have been taking 1-2mg every other day. It is definately doing something.

For example, I had been feeling overstimulated from Racetams and Choline, but adding the Cyprenil seemed to help me get a handle on it and my focus has increased. Placebo effect possibly .....we shall see, but so far I am happy with it.

That is good to hear. One thing to remember whilst taking the Cyprenil is to keep it under the tongue for as long as possible. I would say 10 minutes at the least.

[Advanc3d]

i picked this up on pubmed
now i know why i get a headache of selegiline

OBJECTIVES—The United Kingdom Parkinson's Disease Research Group (UKPDRG) trial found an increased mortality in patients with Parkinson's disease randomised to receive selegiline (10 mg/day) and levodopa compared with those taking levodopa alone. Unwanted effects of selegiline on cardiovascular regulation have been investigated as a potential cause for the unexpected mortality finding of the UKPDRG trial.

METHODS—The cardiovascular responses to a range of physiological stimuli, including standing and head up tilt, were studied in patients with Parkinson's disease receiving levodopa alone and a matched group on levodopa and selegiline.

RESULTS—Head up tilt caused selective and often severe orthostatic hypotension in nine of 16 patients taking selegiline and levodopa, but was without effect on nine patients receiving levodopa alone. Two patients taking selegiline lost consciousness with unrecordable blood pressures and a further four had severe symptomatic hypotension. The normal protective rises in heart rate and plasma noradrenaline were impaired. The abnormal response to head up tilt was reversed by discontinuation of selegiline. Drug withdrawal caused a pronounced deterioration in motor function in 13 of the 16 patients taking selegiline.

CONCLUSION—Therapy with selegiline and levodopa in combination may be associated with severe orthostatic hypotension not attributable to levodopa alone. Selegiline also has pronounced symptomatic motor effects in advanced Parkinson's disease. The possibilities that these cardiovascular and motor findings might be due either to non-selective inhibition of monoamine oxidase or to amphetamine and met-amphetamine are discussed.

http://www.pubmedcen...i?artid=2169684