1. does phenibut interfere with REM sleep? or is it simmilar to ghb and causes REM sleep?
There is suggestion of it; given the associations of other GABAergics and their relative interference with REM, but I am uncertain it is well supported by literature nor will it likely ever be. There is an entire school of thought on the net reporting REM-rebound effects as well. I think this is best fought against with a 5-on, 2-off approach and possibly putting together other agents in the interim for your weekend holiday should you choose to embrace it.
Now, keep in mind that in cases of sleep deprivation, even GABAergics will NOT overcome your body's tendency to not only get to REM quicker, but spend additional time there. So, this is probably more of an "it depends" answer.
2. is phenibut toxic to any organs?
In short, likely not - not even the liver which is often suggested on bb message boards. Phenibut has low acute toxicity (in fact, very low). Reported LD50s (dose required to kill 50% of laboratory animals) are 900 mg/kg i.p. in mice, 700 mg/kg i.p. in rats, and 1000 mg/kg in rats (method of administration not given). Chronic administration of 50 mg/kg did not have teratogenic effects in rats. In clinical studies, no signs of toxicity have been reported, and side effects are few. Some report drowsiness, but this effect is not nearly as likely or severe as with benzodiazepines.
One should be aware of the potential for drug interactions when taking phenibut. In many cases, it will decrease the threshold dose and potentiate certain actions of a drug. It amplifies some of the effects of anesthetics (ether, chloral hydrate, and barbiturates), diazepam, alcohol, and morphine; it would also presumably have an interaction with related drugs, such as other opiates and GHB. In contrast, taking phenibut with some other drugs, such as stimulants, will more than likely just blunt their effect.
In humans, the plasma half-life after a 250 mg oral dose of phenibut is 5.3 hours, and most of the administered drug is excreted unchanged (which is likely why people experience a hangover effect; just due to the long biologic life; people pontificate all over the place that this is secondary to metabolites, blah, blah, blah...without any modification to the drug when looking at excretion data). Reported dosages used in clinical studies range from 250 to 1500 mg daily, usually divided among three doses. Feedback indicates that the ideal dose may be in the higher end of this range.
3. would phenibut case supression of any hormones?
It is suggested as a GH-secretagogue (due mostly to data from close relatives GABA and Baclofen, the latter of which is a chlorinated version of phenibut marketed as a muscle relaxant). If this is truly the case to any significant degree, then long-term use will lead to SUPPRESSION by way of feedback mechanisms inherent to all hormonal systems.
Probably moreso than effects on hormonal systems is data on neurotransmitters. Because of the structural similarity to PEA, phenibut may share some similarities and differences with it. When phenibut is administered along with PEA, it antagonizes many of its effects, such as promotion of anxiety, promotion of seizures, and hyperthermia. This has led some to postulate that antagonism of PEA, rather than the GABA-mimetic activity, may be the important mechanism of action for the anxiolytic effect of phenibut.
Phenibut also increases dopamine levels, and it has been postulated that the structural similarity to PEA may play a role in this effect. If you think about this, you could potentially have suppression of prolactin with dopaminergic agonists, the same as any which would be a neat "side effect" property.
There is one report in the literature of serotonergic effects of phenibut, but it does not look as though this has been followed up on. I mention serotonin because any discussion would be incomplete without talk of the interplay between serotonin and melatonin, which this could play an interesting role in.
D_