NewMind GABAergics bind to and directly or allosterically activate GABA-receptors. GABAergics are a large class of compounds that include pharmacological agents that bear sedative and tranquilizing effects. GABAergic compounds are relevant for researchers involved in neuropharmacological research, particularly into anti-epileptic agents, anxiolytics or hypnotics.

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F-Phenibut FAA, ≥98% F-Phenibut FAA, ≥98%

F-Phenibut FAA, ≥98%

F-Phenibut (Fluorophenibut) is a several-fold more potent derivative of the nootropic and anxiolytic

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F-Phenibut HCl, ≥98% F-Phenibut HCl, ≥98%

F-Phenibut HCl, ≥98%

F-Phenibut (Fluorophenibut) is a several-fold more potent derivative of the nootropic and anxiolytic

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HA-966 HCl, ≥99%HA-966 HCl, ≥99%

HA-966 HCl, ≥99%

Atypical sedative, and neuroprotective antagonist at the glycine modulatory site of the NMDA recepto

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Picamilon sodium, ≥98%Picamilon sodium, ≥98%

Picamilon sodium, ≥98%

Picamilon is a molecule formed by an amide linkage of the vitamin Niacin (vitamin B3, nicotinic acid

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Emoxypine Succinate (Mexidol), ≥98% Emoxypine Succinate (Mexidol), ≥98%

Emoxypine Succinate (Mexidol), ≥98%

Emoxipine and its succinate salt are chemical compounds with antioxidant and membrane-protective pro

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RGPU-95 (p-Cl-Phenylpiracetam), ≥98%RGPU-95 (p-Cl-Phenylpiracetam), ≥98%

RGPU-95 (p-Cl-Phenylpiracetam), ≥98%

RGPU-95 (p-Cl-Phenylpiracetam) is an 5x-10x more potent derivative of the nootropic compound Phenylp

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Details of GABAergics

GABA (gamma aminobutyric acid) and GABA neuron inhibitions are vitally important in the functioning of anxiolytic substances. When we define inhibition – referring to GABA inhibition – we can say that it is a GABAergic modulated decrease in membrane potential such that neuronal transmission is inhibited. Interneurons are also of great importance to GABAergic anxiolytics as they are the production sites for the inhibitory (GABA) and excitatory (glutamate) neurotransmitters in the brain.

Anxiety medication is based on GABAergic function – ie, anxiolytic medications specifically target GABA receptors, affecting neuronal transmission. Medication for anxiety includes the benzodiazepine and barbiturate subgroups, as well as other miscellaneous and naturally-occurring anxiolytic substances.

The negative health effects of anti anxiety medication resulted in increased research into the development of novel anxiolytic agents with better tolerance and decreased interactions. In the search for novel anxiolytics, a new class of compounds was discovered –Phenibut (β-phenyl-γ-aminobutyric acid) and Phenibut-based substances, which were originally sold under prescription in Eastern Europe.2


GABA is the primary inhibitory neurotransmitter in the mammalian brain. This multifunctional neurotransmitter / amino acid is synthesized endogenously from glutamate by the GAD enzyme, as well as through a number of alternative pathways under varying circumstances.

GABA’s primary function is to reduce the possibility of an action potential at synaptic endings, thereby inhibiting neuron transmission. It appears to also have a variety of other functions in tissues and organs throughout the body. Along with glycine, GABA is the key functional inhibitory neurotransmitter.3

GABA is known to counteract the excitatory effects of glutamate and has been proven to have anxiolytic effects at certain concentrations. The exact physiological and biochemical mechanisms of anxiety disorders are still relatively unknown, but GABAergics have been shown to be effective agents in reducing some symptoms of anxiety and, as a result, GABA receptors are often targets for anxiolytic agents.4

Examples of GABA agonists with anxiolytic applications include the benzodiazepine class of chemicals, which are specific to the GABAA receptor subtypes. Other examples include ethanol, clomethiazole, gabapentin and gamma-hydroxybutyrate (GHB).5

There are some circumstances under which GABA can act as a depolarizing (excitatory) neurotransmitter, although this function is rare compared to its inhibitory effects. On the one hand, neurochemical studies have shown that GABA’s inhibitory effects are linked to its ability to hyperpolarize neuronal synapses and decrease the action potential.

On the other hand, GABA’s depolarizing function is linked to the concentration of Cl- ions and membrane permeability. GABA’s excitatory function is observed mostly in developing (immature) cells and may be caused by a different Cl- pump mechanism to adult (mature) cells. Neuronal development relies on the excitatory effects of GABA, which become diminished as cells mature.6

Neuron inhibition

Studies on neuron transmission have confirmed that neurons in the mammalian brain use either glutamate or GABA (g-aminobutyric acid) as the primary neurotransmitter. In effect, GABA and glutamate regulate the excitatory effects of all neuron transmission, and their importance in proper brain physiology and CNS function cannot be overstated.7

GABA and GABAergic substances’ abilities to act as inhibitors of neuron transmission are due to their effects on synaptic action potential. A higher concentration of GABA or a GABAergic substance at the neuron synapse prevents the generation of an action potential, making it less excitatory. While glutamate increases the excitatory postsynaptic potential (EPSP), activation of GABA receptors decreases the resting action potential, resulting in a net inhibitory postsynaptic potential (IPSP).

A typical resting-state neuronal action potential is around -65 to -70 mV. GABA lowers the action potential. When the action potential drops below a threshold level, the neuron is no longer capable of electrochemical signal transduction – and GABA’s inhibitory effect has been realized.8

GABAA vs GABAB receptors

GABA receptors are divided into two functional groups, aptly named the GABAA and GABAB receptor subtypes.

GABAA receptors are the most prominent GABA receptors in the mammalian brain and differ in their pharmacological, electrophysiological, and biochemical properties to the GABAB receptor subtypes. GABAA receptors have been identified in all areas of the brain and are the targets of a large number of GABAergic substances. The GABAA receptor complex mediates a strong increase in membrane conductance (with an equilibrium potential of around -70 mV),9 which often results in membrane hyperpolarization.

Membrane hyperpolarization results in an increased synaptic firing threshold and a decrease in the probability of action potential – resulting in the inhibition of synaptic transmission. GABAA inhibitory effects are facilitated through Cl- ion channels. However, increased Cl- permeability sometimes depolarizes target cells, resulting in an increase in Ca2+ activation and corresponding excitatory effects.10

GABAB receptor effects are always inhibitory and are coupled to G-proteins. There are far fewer GABAB specific ligands than for GABAA and these include Baclofen and Phenibut (β-phenyl-γ-aminobutyric acid). Recent research into GABAB functionality has shown that these receptor subtypes are linked to K+ channels and decrease Ca2+ conductance when activated. Furthermore, GABAB receptors are known to mediate both postsynaptic and presynaptic transmission.11


GABAergic substances have direct or indirect effects on the receptors of the GABA neurotransmitter system. Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the CNS of vertebrate animals and is found throughout the brain. Thus, the early use of GABAergics was developed for anxiolytic benefits due to the efficacy of targeting the ubiquitous GABA receptors.

GABA receptors are divided into two classes: GABAA and GABAB; the former having a ligand-gated ion channel mechanism and the latter being a G-protein coupled receptor (metabotropic receptor).

Endogenous GABA receptor ligands and GABAergic substances bind to either the GABAA or GABAB receptor types to produce inhibitory effects on the CNS and to modulate the glutamatergic system.12

GABAergic substances (GABAergics) have an especially important effect on the inhibitory interneurons found in the mammalian CNS. Inhibitory interneurons are found in varying concentrations throughout the brain and release the neurotransmitters GABA and glycine.13 This is in contrast to the excitatory interneurons which release glutamate and other neuromodulators like acetylcholine.14

The function, therefore, of inhibitory interneurons is the modulation of signal transduction (especially glutamate signal transduction) through the release of the inhibitory neurotransmitter GABA. 2


There are many different classes of anxiolytic substances in both medical and research use today. Anxiolytics are defined as substances that are used to treat symptoms of anxiety. They are usually fast-acting, and often have the potential for addiction. Anxiolytics are prescribed by psychiatrists for the treatment of symptoms of social anxiety, generalized anxiety disorder, and panic attacks.15

Anxiolytics are generally divided into three classes:

  1. Barbiturates
  2. Benzodiazepines
  3. Other anxiolytics, sedatives, and hypnotics

Most anxiolytics act as GABAergics, affecting the GABA neurotransmitter system to reduce symptoms of anxiety.

Barbiturates, for example, are a class of substances that are derived from barbituric acid and have a nonspecific enhancing effect on GABA transmission. Barbiturates were once used as treatments for anxiety, epilepsy, and as anesthetics. Today, this class of compounds has largely been replaced by safer chemicals.16

Benzodiazepines act as GABAA receptor agonists. Benzodiazepines target GABAA subtype proteins, changing the receptor configuration to allow Cl- entry into the neuron and thereby lowering the action potential.

he benzodiazepines are a large class of chemical compounds with great variance in their mechanisms of action as well as potency and duration of effects. All have the potential for abuse. Benzodiazepines are also used in the treatment of panic attacks, seizures, and sleep disorders.17

Not all anxiolytic agents are laboratory-made chemicals. Numerous plant extracts and dietary supplements have been discovered as having potent anxiolytic effects. Examples of herbal and dietary anxiolytic agents include:

  1. St John’s Wort (Hypericum perforatum)
  2. Ginkgo biloba
  3. Ashwagandha (Withania somnifera)
  4. Kava
  5. Valerian (Valeriana officiaonalis)
  6. L-Theanine
  7. Vitamin C18

GABAergics / Anxiolytics on Newmind

F-Phenibut, also known as Fluorophenibut, Fluoribut, is a derivative of the GABAB receptor ligand, Phenibut. Studies have demonstrated that F-Phenibut has a potency that is several-fold higher than that of Phenibut in both behavioral effects and GABAB receptor affinity.19

Phenibut is an atypical Nootropic and anxiolytic with potent GABAB receptor activity, similar to Baclofen (β-(4-chlorophenyl)-GABA) and pregabalin (β-isobutyl-GABA). Phenibut works not only as a GABAB-receptor agonist but also as an inhibitor of α2δ subunit-containing voltage-gated calcium channels.20

Toxicity and Warnings

Most anxiolytics have a strong potential for abuse – especially benzodiazepine and barbiturate-like substances. Anxiolytics and GABAergics also tend to have strong interactions with other medications and chemical substances, especially ethanol (alcohol), which acts as a potent GABAA agonist.

GABAergic interactions can lead to serious health complications including respiratory failure, coma, and death. For more information about the toxicity of Newmind anxiolytics and GABAergics, please read through the specific product write-up.

It is important to note that most research chemicals, including those available for purchase on NewMind, lack an established human toxicity rating. More importantly, ALL compounds offered on NewMind are strictly NOT for human consumption.

1 DJ Sanger, “GABA and the behavioral effects of anxiolytic drugs”, Life Sci. 1985 Apr 22;36(16):1503-13.

2 I Lapin, “Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug”, CNS Drug Rev. 2001 Winter;7(4):471-81.

3 M Watanabe et al., “GABA and GABA receptors in the central nervous system and other organs”, Int Rev Cytol. 2002;213:1-47.

4 RB Lydiard, “The role of GABA in anxiety disorders”, J Clin Psychiatry. 2003;64 Suppl 3:21-7.

5 F Caputo, M Bernardi, “Medications acting on the GABA system in the treatment of alcoholic patients”, Curr Pharm Des. 2010;16(19):2118-25

6 NC Spitzer, “How GABA generates depolarization”, J Physiol. 2010 Mar 1; 588(Pt 5): 757–758, doi: 10.1113/jphysiol.2009.183574

7 SM Paul, “GABA and Glycine”, Neuropsychopharmacology: The Fifth Generation of Progress, 2000, available online, retrieved on April 5, 2017

8 “GABA Neurotransmitter”, DNA Learning Center, Cold Spring Harbor Laboratory, available online, retrieved on April 5, 2017

9 “Neurobiology – resting potential and chloride channels”, Rudolf Cardinal, 4 Feb 99, Psychology note, available online, retrieved on April 5, 2017

10 X Leinekugel et al., “Ca2+ oscillations mediated by the synergistic excitatory actions of GABA(A) and NMDA receptors in the neonatal hippocampus”, Neuron. 1997 Feb;18(2):243-55.

11 CL Padgett, PA Slesinger, “GABAB receptor coupling to G-proteins and ion channels”, Adv Pharmacol. 2010;58:123-47. doi: 10.1016/S1054-3589(10)58006-2.

12 R Mitchell et al., “Endogenous GABA receptor ligands in hypophysial portal blood”, Neuroendocrinology. 1983 Sep;37(3):169-76.

13 C Kelsom and W Lu, “Development and specification of GABAergic cortical interneurons”, Cell & Bioscience 20133:19, DOI: 10.1186/2045-3701-3-19

14 JT Buchanan and S Grillner, “Newly identified "glutamate interneurons" and their role in locomotion in the lamprey spinal cord”, Science, vol. 236, 1987, p. 312+. Academic OneFile, Accessed 5 Apr. 2017

15 “Anxiolytics”,, retrieved on April 5, 2017

16 “Barbiturates”,, retrieved April 5, 2017

17 “Benzodiazepines”,, retrieved April 5, 2017

18 E Alramadhan et al., “Dietary and botanical anxiolytics”, Med Sci Monit. 2012; 18(4): RA40–RA48, doi: 10.12659/MSM.882608

19 NG Bowery et al., “Characteristics of GABAB receptor binding sites on rat whole brain synaptic membranes”, British Journal of Pharmacology BJP, Volume 78, ssue 1, January 1983, Pages 191–206

20 L Zvejniece et al., “R-phenibut binds to the α2-δ subunit of voltage-dependent calcium channels and exerts gabapentin-like anti-nociceptive effects”, Pharmacol Biochem Behav. 2015 Oct;137:23-9. doi: 10.1016/j.pbb.2015.07.014. Epub 2015 Jul 31.