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    Ghrp6

    How much do you have to take to up your hunger . Nothing works


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    Quote Originally Posted by Frankdoz View Post
    How much do you have to take to up your hunger . Nothing works


    Sent from my iPhone using Tapatalk
    100-150mcg is all you really need on a empty stomach.

    Have you ever tried some Cyprohetadine (Practin) 4mg?

    Practin 4mg Tablet belongs to a group of medicines called antihistamines. It is used in the treatments of various allergic conditions. It relieves symptoms like itching, swelling and rashes. It is also used to treat loss of appetite (need for food)

    Years ago back in the early 90's we use to take a Dbol out of Dominican Republic (Anabolex) that was partial dbol and partial Practin. These would make you so hungry all you would want to do is eat and sleep.
    Great to assist with hunger, I think it's better in that respect compared to GHRP's with hunger pangs.. GHRP's give you a false sense of going hypo. Practin just makes you hungry as all hell with no shaky feeling, just hardcore legit desire to eat non stop like a machine.

    It goes amazingly well with oral AAS..

    http://www.anabolicsteroidforums.com...hlight=Practin

    Practin TD (appetite stimulation drug)
    Does orals suppress your appetite (dbol/drol).. They do me, that's for sure..
    Try adding this to your AAS combo..
    Cyproheptadine is a antihistamine, but it has been used for off label properties with treating conditions, syndromes in people that have little to no appetite due to whatever issues that may have trigger the appetite loss.
    Back in the late 90's early 2000's some pharma companies would in fact add this to their Dbol, yup, that's right.. Guy's were blowing up like craziness..
    I decided to add this once again due to my script meds interfering with my appetite , this will give me the added advantage with wanting to pound some food during difficult times..
    Please do NOT PM me for source.. You can get these from just about any legit ONLINE pharma dispensary, you do need a script for most, but some don't require it.

    2 x 4mg tabs is all you really need, take with your orals (dbol/drol).. take 1 in am and 1 in pm.




  3. #3
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    Sweet thx bro


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    Quote Originally Posted by Frankdoz View Post
    Sweet thx bro


    Sent from my iPhone using Tapatalk
    Also so more..


    http://www.anabolicsteroidforums.com/threads/80969-Depression-appetite-Solution-for-those-that-suffer%21?highlight=increase+appetite

    Depression/appetite..Solution for those that suffer!

    As some of you know, well the mostly the members that speak to me on a personal level know that I have had my bouts with depression here and there, and trying medication after medication throughout the years..
    Often at times when I have a low my appetite naturally takes a hit as well, and struggling to choke down food all the while trying to have a stable steady keel with my outlook..

    Last summer I introduced a drug that I was kinda unfamiliar with (just recently re-added it again,glad I did), but did some research on it, and it turned out to be the Swiss army knife of antidepressants... Its role is multi-functional, at the same time not effecting sex drive,libido, ability to cum, or anything that SSIR's do to people..

    This drug has been a life saver, not only does it treat my depression like symptoms, but it knocks me the hell out like an ambien would (deep sleep wise)..Further more, its been used to treat people with wasting disorders where they cant eat, or lack of appetite, anorexia..In fact its one of the top 3 most prescribed for treating appetite stimulation.. Dosages will vary.. I started at 30mgs and I was blown away on how well I was sleeping, and the increase and desire to eat was out of this world, it actually became problematic at night lol... I now take the max dosage at 45mgs, sleep is sound, and appetite has been like that or a carnivore.

    side effects? zero for me.... maybe a bit groggy upon waking up, but nothing a dark roast can't fix...

    Its a great alternative to the other crap those Dr have pushed on me for years..Here's some info below, I hope this can assist anyone out there..

    Mirtazapine, sold under the brand name Remeron among others, is an
    atypical antidepressant which is used primarily in the treatment of depression.[7] In addition to its antidepressant properties, mirtazapine has anxiolytic, sedative, antiemetic, and appetite stimulant effects and is sometimes used in the treatment of anxiety disorders, insomnia, nausea and vomiting, and to produce weight gain when desirable.[7][8] It is taken by mouth.
    The drug acts as an
    antagonist of certain adrenergic and serotonin receptors, and is also a strong antihistamine.[7] It is sometimes described as a noradrenergic and specific serotonergic antidepressant (NaSSA),[7] although the actual evidence in support of this label has been regarded as poor.[9] Chemically, mirtazapine is a tetracyclic antidepressant (TeCA), with four interconnected rings of atoms, and is a relative of the TeCA mianserin(Tolvon).[10][11]
    Mirtazapine was developed by
    Organon International in the Netherlands and was introduced in the United States in 1996.[4] Its patent expired in 2004, so generic versions are available.[12]


    Approved and off-label[edit]

    Mirtazapine's primary use is the
    treatment of major depressive disorder and other mood disorders.[13][14]
    However, it has also been found useful in alleviating the following conditions and is sometimes prescribed off-label for their treatment:







    Effectiveness and tolerability[edit]

    In 2010
    NICE published a guideline for treating depression that included a review of antidepressants. It recommended generic SSRIs as first line choices, as they are "equally effective as other antidepressants and have a favourable risk–benefit ratio."[29] With respect to mirtazapine, it found: "There is no difference between mirtazapine and other antidepressants on any efficacy measure, although in terms of achieving remission mirtazapine appears to have a statistical though not clinical advantage. In addition, mirtazapine has a statistical advantage over SSRIs in terms of reducing symptoms of depression, but the difference is not clinically important. However, there is strong evidence that patients taking mirtazapine are less likely to leave treatment early because of side effects, although this is not the case for patients reporting side effects or leaving treatment early for any reason."[30]
    A 2011 Cochrane review that compared mirtazapine to other antidepressants, found that while it appears to have a faster onset in people for whom it works (measured at 2 weeks), it is about the same as other antidepressants at 6 weeks.
    [31]
    A 2012 review focused on antidepressants and sleep found that in many people with sleep disorders caused by depression, mirtazapine reduces the time it takes to fall asleep and increases the quality of sleep, but that in some people it can disturb sleep, causing
    restless leg syndrome in 8 to 28% of people, and in rare cases causes REM sleep behavior disorder.[32]
    A 2018 systematic review and network meta-analysis comparing the efficacy and acceptability of 21 antidepressant drugs showed mirtazapine to be one of the most effective antidepressants in head-to-head studies.
    [33]
    In general, all antidepressants, including mirtazapine, require at least a week for their therapeutic benefits on depressive and anxious symptoms to become apparent.
    [34][35]
    Side effects[edit]

    A 2011 Cochrane review found that compared with other antidepressants, it is more likely to cause weight gain and sleepiness, but it is less likely to cause tremor than tricyclic antidepressants, and less likely to cause nausea and sexual dysfunction than SSRIs.
    [31]
    Very common (≥10% incidence) adverse effects include constipation, dry mouth, sleepiness, increased appetite and weight gain.
    [4][5][6][36][37][38][39][40][41]
    Common (1–10% incidence) adverse effects include weakness, confusion, dizziness,
    peripheral edema, and negative lab results like elevated transaminases, elevated serum triglycerides, and elevated total cholesterol.[6]
    Mirtazapine is not considered to have a risk of many of the side effects often associated with other antidepressants like the SSRIs, and may actually improve certain ones when taken in conjunction with them.
    [7][42] (Those adverse effects include decreased appetite, weight loss, insomnia, nausea and vomiting, diarrhoea, urinary retention, increased body temperature, excessive sweating, pupil dilation and sexual dysfunction.[7][42])
    In general, some antidepressants, especially SSRIs, can paradoxically exacerbate some peoples' depression or anxiety or cause
    suicidal ideation.[43] Despite its sedating action, mirtazapine is also believed to be capable of this, so in the United States and certain other countries, it carries a black box label warning of these potential effects.
    A case report published in 2000 noted an instance in which mirtazapine counteracted the action of
    clonidine, causing a dangerous rise in blood pressure.[44]
    Discontinuation[edit]

    Mirtazapine and other antidepressants may cause a
    discontinuation syndrome upon cessation.[7][45][46] A gradual and slow reduction in dose is recommended to minimize discontinuation symptoms.[47] Effects of sudden cessation of treatment with mirtazapine may include depression, anxiety, panic attacks, vertigo, restlessness, irritability, decreased appetite, insomnia, diarrhea, nausea, vomiting, flu-like symptoms such as allergies and pruritus, headaches and sometimes hypomania or mania.[45][48][49][50][51]
    Overdose[edit]

    Mirtazapine is considered to be relatively safe in the event of an
    overdose,[35] although it is considered slightly more toxic in overdose than most of the SSRIs (except citalopram).[52] Unlike the tricyclic antidepressants, mirtazapine showed no significant cardiovascularadverse effects at 7 to 22 times the maximum recommended dose.[42] Case reports of overdose with as much as 30 to 50 times the standard dose described the drug as relatively nontoxic, compared to tricyclic antidepressants.[53][54]
    Twelve reported fatalities have been attributed to mirtazapine overdose.
    [55][56] The fatal toxicity index (deaths per million prescriptions) for mirtazapine is 3.1 (95% CI: 0.1 to 17.2). This is similar to that observed with SSRIs.[57]
    Interactions[edit]

    Concurrent use with inhibitors or inducers of the
    cytochrome (CYP) P450isoenzymesCYP1A2, CYP2D6, and/or CYP3A4 can result in altered concentrations of mirtazapine, as these are the main enzymes responsible for its metabolism.[3][7] As examples, fluoxetine and paroxetine, inhibitors of these enzymes, are known to modestly increase mirtazapine levels, while carbamazepine, an inducer, considerably decreases them.[3]Liver and moderate renal impairment have been reported to decrease the oral clearance of mirtazapine by about 30%; severe renal impairment decreases it by 50%.[3]
    According to information from the manufacturers, mirtazapine should not be started within two weeks of any
    monoamine oxidase inhibitor (MAOI) usage; likewise, MAOIs should not be administered within two weeks of discontinuing mirtazapine.[58] Mirtazapine in combination with an SSRI, SNRI, or TCA as an augmentation strategy is considered to be relatively safe and is often employed therapeutically,[42] with a combination of venlafaxine and mirtazapine, sometimes referred to as "California rocket fuel".[59][60]
    Pharmacology[edit]

    Pharmacodynamics[edit]

    See also: Pharmacology of antidepressants and Tetracyclic antidepressant § Pharmacology
    Site Ki (nM) Species Ref
    SERT >10,000 Human [62][63]
    NET ≥4,600 Human [10][62]
    DAT >10,000 Human [62][63]
    5-HT1A 3,330–5,010 Human [63][7]
    5-HT1B 3,534–12,600 Human [63][7]
    5-HT1D 794–5,010 Human [63][7]
    5-HT1E 728 Human [63]
    5-HT1F 583 Human [63]
    5-HT2A 6.3–69 Human [7][64][63]
    5-HT2B 200 Human [7]
    5-HT2C 8.9–39 Human [64][7][63]
    5-HT3 7.9 Human [7]
    5-HT4L >10,000 Human [63]
    5-HT5A 670 Human [63]
    5-HT6 ND ND ND[63]
    5-HT7 265 Human [64][63]
    α1A 316–1,815 Human [63][63]
    α2A 20 Human [64][63]
    α2B 88 Human [63]
    α2C 18 Human [64][63]
    β >10,000 Human [63]
    D1 4,167 Rat [64]
    D2 >5,454 Human [64][63]
    D3 5,723 Human [64][63]
    D4 2,518 Human [63]
    H1 0.14–1.6 Human [65][64][7][63]
    H2 >10,000 Rat [66][65]
    H3 83,200 Human [65]
    H4 >100,000 Human [65]
    mACh 670 Human [7][10]
    VGSC 6,905 Rat [63]
    VDCC >10,000 Rat [63]
    Values are Ki (nM). The smaller the value, the more strongly the drug binds to the site.


    Mirtazapine has antihistamine, α2-blocker, and antiserotonergic activity.[7][67] It is specifically a potent antagonist or inverse agonist of the α2A-, α2B-, and α2C-adrenergic receptors, the serotonin5-HT2A, 5-HT2C, and 5-HT3receptors, and the histamineH1 receptor.[7][67] Unlike many other antidepressants, it does not inhibit the reuptake of serotonin, norepinephrine, or dopamine,[7][67] nor does it inhibit monoamine oxidase.[68] Similarly, mirtazapine has weak or no activity as an anticholinergic or blocker of sodium or calcium channels, in contrast to most TCAs.[7][67][63] In accordance, it has better tolerability and low toxicity in overdose.[7][69] As an H1 receptor antagonist, mirtazapine is extremely potent, and is in fact the most potent of all the TCAs and TeCAs.[10][70][71] Antagonism of the H1 receptor is by far the strongest activity of mirtazapine, with the drug acting as a selective H1receptor antagonist at low concentrations.[7][63]
    The (S)-(+) enantiomer of mirtazapine is responsible for antagonism of the serotonin 5-HT2A and 5-HT2C receptors,
    [11] while the (R)-(–) enantiomer is responsible for antagonism of the 5-HT3 receptor.[11] Both enantiomers are involved in antagonism of the H1 and α2-adrenergic receptors,[11][5] although the (S)-(+) enantiomer is the stronger antihistamine.[72]
    Although not clinically relevant, mirtazapine has been found to act as a
    partial agonist of the κ-opioid receptor at high concentrations (EC50 = 7.2 μM).[73]
    α2-Adrenergic receptor[edit]

    Antagonism of the α2-adrenergic receptors, which function largely as
    inhibitoryautoreceptors and heteroreceptors, enhances adrenergic and serotonergicneurotransmission, notably central5-HT1A receptor mediated transmission in the dorsal raphe nucleus and hippocampus; hence, mirtazapine's classification as a NaSSA. Indirect α1 adrenoceptor-mediated enhancement of serotonin cell firing and direct blockade of inhibitory α2heteroreceptors located on serotonin terminals are held responsible for the increase in extracellular serotonin.[7][13][74][75][76] Because of this, mirtazapine has been said to be a functional "indirect agonist" of the 5-HT1Areceptor.[75] Increased activation of the central 5-HT1A receptor is thought to be a major mediator of efficacy of most antidepressant drugs.[77]
    5-HT2 and 5-HT3 receptors[edit]

    Antagonism of the 5-HT2 subfamily of receptors and inverse agonism of the 5-HT2C receptor appears to be in part responsible for mirtazapine's efficacy in the treatment of depressive states.
    [78][79] Mirtazapine increases dopamine release in the prefrontal cortex.[80][81] Accordingly, it was shown that by blocking the α2-adrenergic receptors and 5-HT2C receptors mirtazapine disinhibited dopamine and norepinephrine activity in these areas in rats.[82] In addition, mirtazapine's antagonism of 5-HT2A receptors has beneficial effects on anxiety, sleep and appetite, as well as sexual function regarding the latter receptor.[7][42] Mirtazapine has been shown to lower drug seeking behaviour in various human and animal studies.[83][84][85] It is also being investigated in substance abuse disorders to reduce withdrawal effects and improve remission rates.[83][86][87][88]
    Antagonism of the 5-HT3 receptor, an action mirtazapine shares with the approved antiemetic
    ondansetron, significantly improves pre-existing symptoms of nausea, vomiting, diarrhea, and irritable bowel syndrome in afflicted individuals.[89] Mirtazapine may be used as an inexpensive antiemetic alternative to ondansetron.[24] Blockade of the 5-HT3 receptors has also shown to improve anxiety and to be effective in the treatment of drug addiction in several studies.[90] In conjunction with substance abuse counseling, mirtazapine has been investigated for the purpose of reducing methamphetamine use in dependent individuals with success.[84] In contrast to mirtazapine, the SSRIs, SNRIs, MAOIs, and some TCAs increase the general activity of the 5-HT2A, 5-HT2C, and 5-HT3 receptors leading to a host of negative changes and side effects, the most prominent of which including anorexia, insomnia, sexual dysfunction (loss of libido and anorgasmia), nausea, and diarrhea, among others. As a result, it is often combined with these drugs to reduce their side-effect profile and to produce a stronger antidepressant effect.[42][91]
    Mirtazapine does not have
    serotonergic activity and does not cause serotonergic side effects or serotonin syndrome.[9][92] This is in accordance with the fact that it is not a serotonin reuptake inhibitor or MAOI, nor a serotonin receptor agonist.[9][92] There are no reports of serotonin syndrome in association with mirtazapine alone, and mirtazapine has not been found to cause serotonin syndrome in overdose.[9][92][93] However, there are a handful of case reports of serotonin syndrome occurring with mirtazapine in combination with serotonergic drugs like SSRIs, although such reports are unusual, very rare, and do not necessarily implicate mirtazapine as causative.[9][94][95][96][97][98] The addition of mirtazapine to an MAOI does not cause serotonin syndrome, and has been considered to be a safe combination.[9][92] Moreover, mirtazapine may actually be useful in the treatment of serotonin syndrome, with at least one publication finding it to be effective in resolving the syndrome.[9][99][100] This is in accordance with the fact that the 5-HT2A receptor is the predominant serotonin receptor thought to be involved in the pathophysiology of serotonin syndrome (with the 5-HT1A receptor seeming to be protective).[9][92] Mirtazapine is a potent 5-HT2A receptor antagonist, and cyproheptadine, a drug that shares this property, mediates recovery from serotonin syndrome and is well-established clinically as an antidote against it.[9][101]
    H1 receptor[edit]

    Mirtazapine is a very strong H1 receptor inverse agonist and, as a result, it can cause powerful
    sedative and hypnotic effects.[7] A single 15 mg dose of mirtazapine to healthy volunteers has been found to result in over 80% occupancy of the H1 receptor and to induce intense sleepiness.[72] After a short period of chronic treatment, however, the H1 receptor tends to desensitize and the antihistamine effects become more tolerable. Many patients may also dose at night to avoid the effects, and this appears to be an effective strategy for combating them. Blockade of the H1 receptor may improve pre-existing allergies, pruritus, nausea, and insomnia in afflicted individuals. It may also contribute to weight gain, however. In contrast to the H1 receptor, mirtazapine has only low affinity for the muscarinic acetylcholine receptors, although anticholinergic side effects like dry mouth, constipation, and mydriasis are still sometimes seen in clinical practice.[102]
    Pharmacokinetics[edit]

    The
    oralbioavailability of mirtazapine is about 50%. It is found mostly bound to plasma proteins, about 85%. It is metabolized primarily in the liver by demethylation and hydroxylation via cytochrome P450enzymes. One of its major metabolites is desmethylmirtazapine. The overall elimination half-life is 20–40 hours. About 15% is eliminated in feces and 75% in urine.[103]:430
    History[edit]

    Mirtazapine was first synthesized at
    Organon and published in 1989, was first approved for use in major depressive disorder in the Netherlands in 1994, and was introduced in the United States in 1996 under the brand name Remeron.[103]:429[104][105]
    Society and culture[edit]


    A 15 mg tablet of generic mirtazapine.

    Generic names[edit]

    Mirtazapine is the
    English and Frenchgeneric name of the drug and its INN, USAN, USP, BAN, DCF, and JAN.[1][2][106] Its generic name in Spanish is mirtazapina, in German is Mirtazapin, and in Latin is mirtazapinum.[1][2]
    Brand names[edit]

    Mirtazapine is marketed under many brand names worldwide, including Adco-Mirteron, Afloyan, Amirel, Arintapin Smelt, Avanza, Azapin, Beron, Bilanz, Calixta, Ciblex, Combar, Comenter, Depreram, Divaril, Esprital, Maz, Menelat, Mepirzapine, Merdaten, Meronin, Mi Er Ning, Milivin, Minelza, Minivane, Mirastad, Mirazep, Miro, Miron, Mirrador, Mirt, Mirta, Mirtabene, Mirtadepi, Mirtagamma, Mirtagen, Mirtalan, Mirtamor, Mirtamylan, Mirtan, Mirtaneo, Mirtapax, Mirtapil, Mirtapine, Mirtaron, Mirtastad, Mirtax, Mirtaz, Mirtazap, Mirtazapin, Mirtazapina, Mirtazapine, Mirtazapinum, Mirtazelon, Mirtazon, Mirtazonal, Mirtel, Mirtimash, Mirtin, Mirtine, Mirzapine, Mirzaten, Mirzest, Mitaprex, Mitaxind, Mitocent, Mitrazin, Mizapin, Motofen, Mytra, Norset, Noxibel, Pharmataz, Promyrtil, Ramure, Redepra, Reflex, Remergil, Remergon, Remeron, Remirta, Rexer, Saxib, Sinmaron, Smilon, Tazepin, Tazimed, Tetrazic, Tifona, U-Mirtaron, U-zepine, Valdren, Vastat, Velorin, Yarocen, Zania, Zapex, Zestat, Zismirt, Zispin, Zuleptan, and Zulin.
    [2]
    Chemistry[edit]

    Mirtazapine is a
    tetracyclic piperazinoazepine; mianserin was developed by the same team of organic chemists and mirtazapine differs from it via addition of a nitrogen atom in one of the rings.[103]:429[107][108] It is a racemic mixture of enantiomers. The (S)-(+)-enantiomer is known as esmirtazapine.
    Analogues of mirtazapine include mianserin, setiptiline, and aptazapine.
    Synthesis[edit]

    A
    chemical synthesis of mirtazapine has been published.[109]
    Research[edit]

    The use of mirtazapine has been explored in several additional conditions:






    Veterinary use[edit]

    Mirtazapine is sometimes prescribed as an appetite stimulant for cats or dogs experiencing anorexia due to medical conditions such as
    chronic kidney disease. It is especially useful for treating combined poor appetite and nausea in cats and dogs.[123][124]

  5. #5
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    I have bad indigestion which causes me not to be hungry just nauseous. Which sucks even when I use eq.


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  6. #6
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    GHRP6 will spike your hunger for like 20 or 30 minutes and that’s it. It’s good to get a single meal down. I’m just starting mk677 which is supposed to give you extra hunger throughout the day. We’ll see how that goes.
    As far as the indigestion goes, you could try what I just did recently that helped me. Get some good probiotics and some good digestive enzymes. Yes you should focus on your appetite but you should also focus on your digestion. The better you digest your food the better your appetite will be.

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    GHRP6 is great for running Orals that kill your appetite. It does only last like a hour but fuck it it works and is cheap as fuck.

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