Moclobemide

Strike me lucky

Well-Known Member
Been a few posts on moclobemide. It has been on my list to try for many years but other things keep popping up. Its not a cure but a good improvement would be great. It seems to help energy and improve mood. Both would be helpful at the moment. If it helps post herpetic neuralgia would be good.

It seems to have less side effects . apparently. My main concern is disruptive sleep but generally its dosed twice a day, im thinking on starting at dosing once a day to start with.

Im interested in others experiences or any interesting informative links .

Cheers
 

Remy

Administrator
It's been on my list for a while too...but keeps getting pushed down for some reason.

My doctor is not a fan of MAOIs at all so that is probably some of it for me. But selective ones seem much safer, no food restrictions etc.

Be curious to hear about experiences with it too!
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
I didn't know anything about it. Wikipedia says it's not approved in the U.S. I tend to disregard the mood aspects of "antidepressants" now because they clearly affect so many other parts of the body.

Moclobemide (sold as Amira, Aurorix,[7] Clobemix , Depnil and Manerix[8]) is a reversible inhibitor of monoamine oxidase A (RIMA) drug primarily used to treat depression and social anxiety.[9][10][11] It is not approved for use in the United States,[12] but is approved in other Western countries such as the UK[11] and Australia (TGA approved in December 2000).[13


Check this out:

Moclobemide may also have benefit for some patients with Parkinson's Disease by extending and enhancing the effects of l-dopa.

Definitely keep L-dopa in mind...Can't say anymore than that right now...:rolleyes: - but kept it in mind.

This isn't bad news either:

Additionally moclobemide was found, unlike most other antidepressants on the market, to actually improve all aspects of sexual function.:wacky:

It is the only reversible MAOI in use in clinical practice.[8] The fact that moclobemide's pharmacokinetic properties are unaltered by age, that cognition is improved in the elderly, and moclobemide has low potential for food and drug interactions opened up a new avenue for the treatment of major depressive disorder
Interesting drug! :hungry:
 

Remy

Administrator
I looked back at my notes on moclobemide today and found this study:

Brain Res. 2007 Mar 23;1138:30-8. Epub 2007 Jan 9.
Moclobemide attenuates anoxia and glutamate-induced neuronal damage in vitro independently of interaction with glutamate receptor subtypes.

Verleye M1, Steinschneider R, Bernard FX, Gillardin JM.

Abstract

Recent data suggested the existence of a bidirectional relation between depression and neurodegenerative diseases resulting from cerebral ischemia injury.

Glutamate, a major excitatory neurotransmitter, has long been recognised to play a key role in the pathophysiology of anoxia or ischemia, due to its excessive accumulation in the extracellular space and the subsequent activation of its receptors.

A characteristic response to glutamate is the increase in cytosolic Na(+) and Ca(2+) levels which is due mainly to influx from the extracellular space, with a consequent cell swelling and oxidative metabolism dysfunction.

The present study examined the in vitro effects of the antidepressant and type-A monoamine oxidase inhibitor, moclobemide, in neuronal-astroglial cultures from rat cerebral cortex exposed to anoxia (for 5 and 7 h) or to glutamate (2 mM for 6 h), two in vitro models of brain ischemia. In addition, the affinity of moclobemide for the different glutamate receptor subtypes and an interaction with the cell influx of Na(+) and of Ca(2+) enhanced by veratridine and K(+) excess, respectively, were evaluated. Moclobemide (10-100 microM) included in the culture medium during anoxia or with glutamate significantly increased in a concentration-dependent manner the amount of surviving neurons compared to controls. Moclobemide displayed no binding affinity for the different glutamate receptor subtypes (IC(50)>100 microM) and did not block up to 300 microM the entry of Na(+) and of Ca(2+) activated by veratridine and K(+), respectively.

These results suggest that the neuroprotective properties of moclobemide imply neither the glutamate neurotransmission nor the Na(+) and Ca(2+) channels.
So if my working theory is correct, that glutamate causes an increase in intracellular calcium which causes oxidative stress and results in symptoms, then this drug may not be the best one to choose to get the calcium out of the cell because it doesn't block its entry.

It may offer other benefits though. It's hard to know without trying it. As usual. :rolleyes:
 

Snow Leopard

Active Member
The benefits seem rather modest, but it is something worth considering:

http://www.ncbi.nlm.nih.gov/pubmed/11030484
J Clin Psychiatry. 2000 Sep;61(9):643-8.
A randomized, double-blind placebo-controlled trial of moclobemide in patients with chronic fatigue syndrome.

Hickie IB1, Wilson AJ, Wright JM, Bennett BK, Wakefield D, Lloyd AR.
METHOD:

Ninety patients with chronic fatigue syndrome, diagnosed with our system that approximates CDC criteria, participated in a randomized, placebo-controlled, double-blind trial of 450 to 600 mg/day of moclobemide, a novel reversible inhibitor of monoamine oxidase-A.
RESULTS:

Fifty-one percent (24/47) of patients receiving moclobemide improved compared with 33% (14/43) of patients receiving placebo (odds ratio = 2.16, 95% confidence interval [CI] = 0.9 to 5.1). Drug response was best characterized symptomatically by an increase in the subjective sense of vigor and energy rather than a reduction in depressed mood. The effect of moclobemide on subjective energy was detectable within the first 2 weeks of treatment and increased across the course of the study. The greatest reduction in clinician-rated disability was in patients with concurrent immunologic dysfunction (mean difference in standardized units of improvement = 0.8, 95% CI = 0.03 to 1.6).
CONCLUSION:

Moclobemide produces some improvement in key symptoms experienced by patients with chronic fatigue syndrome. This effect is not dependent on the presence of concurrent psychological distress and is likely to be shared with other monoamine oxidase inhibitors.
 

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