Kavain (K)
Kavain, known as “K” or the number 4 on kava chemo types is one of, if not the most studied and pharmacologically important kavalactones in the plant. The initial resorption time of orally applied kavain was around 15 minutes, and kavain’s half-life in the body has been shown to be about 9 hours [1]. Kavain has long thought to be the constituent of kava that causes a euphoric uplifting, yet calming effect. Being the most sought after kavalactone, kavain typically resides in the first 2 positions of a noble kava’s chemotype. Its direct physical actions include inhibiting voltage-gated sodium channels in neurons, and potentiating GABA ligand binding. Kava has been thought to act similarly to benzodiazepines, however none of these studies detected significant affinity of kavalactones for the benzodiazepine binding site, contrary to popular belief [2]. Kavain has been shown to have a number of interesting functions. Studies have shown anti-inflammatory effects, cancer reduction [3], anxiety reduction [4], MOA-B inhibition [5], Parkinson’s symptoms reduction, and neuroprotection [6]. The list for beneficial effects of this compound is long, and topics related to it are still being researched even today.
[1] Tarbah F, Mahler H, Kardel B, Weinmann W, Hafner D, Daldrup T. Kinetics of kavain and its metabolites after oral application. J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Jun 5;789(1):115-30. doi: 10.1016/s1570-0232(03)00046-1. PMID: 12726850.
[2] Chua HC, Christensen ETH, Hoestgaard-Jensen K, Hartiadi LY, Ramzan I, et al. (2016) Kavain, the Major Constituent of the Anxiolytic Kava Extract, Potentiates GABAA Receptors: Functional Characteristics and Molecular Mechanism. PLOS ONE 11(6): e0157700. https://doi.org/10.1371/journal.pone.0157700
[3] Xiaoren Tang and Salomon Amar. "Kavain inhibition of LPS-induced TNF-α via ERK/LITAF." Royal Society of Chemistry, Toxicol. Res., 2016, 5, 188-196
[4] Singh, Y. N., & Singh, N. N. (2002). Therapeutic Potential of Kava in the Treatment of Anxiety Disorders. CNS Drugs, 16(11), 731-743. doi:10.2165/00023210-200216110-00002
[5] Prinsloo, D., Dyk, S. V., Petzer, A., & Petzer, J. P. (2019). Monoamine Oxidase Inhibition by Kavalactones from Kava (Piper Methysticum). Planta Medica, 85(14/15), 1136-1142. doi:10.1055/a-1008-9491
[6] Schmidt N, Ferger B. Neuroprotective effects of (+/-)-kavain in the MPTP mouse model of Parkinson's disease. Synapse. 2001 Apr;40(1):47-54. doi: 10.1002/1098-2396(200104)40:1<47::AID-SYN1025>3.0.CO;2-S. PMID: 11170221.
Kavain, known as “K” or the number 4 on kava chemo types is one of, if not the most studied and pharmacologically important kavalactones in the plant. The initial resorption time of orally applied kavain was around 15 minutes, and kavain’s half-life in the body has been shown to be about 9 hours [1]. Kavain has long thought to be the constituent of kava that causes a euphoric uplifting, yet calming effect. Being the most sought after kavalactone, kavain typically resides in the first 2 positions of a noble kava’s chemotype. Its direct physical actions include inhibiting voltage-gated sodium channels in neurons, and potentiating GABA ligand binding. Kava has been thought to act similarly to benzodiazepines, however none of these studies detected significant affinity of kavalactones for the benzodiazepine binding site, contrary to popular belief [2]. Kavain has been shown to have a number of interesting functions. Studies have shown anti-inflammatory effects, cancer reduction [3], anxiety reduction [4], MOA-B inhibition [5], Parkinson’s symptoms reduction, and neuroprotection [6]. The list for beneficial effects of this compound is long, and topics related to it are still being researched even today.
[1] Tarbah F, Mahler H, Kardel B, Weinmann W, Hafner D, Daldrup T. Kinetics of kavain and its metabolites after oral application. J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Jun 5;789(1):115-30. doi: 10.1016/s1570-0232(03)00046-1. PMID: 12726850.
[2] Chua HC, Christensen ETH, Hoestgaard-Jensen K, Hartiadi LY, Ramzan I, et al. (2016) Kavain, the Major Constituent of the Anxiolytic Kava Extract, Potentiates GABAA Receptors: Functional Characteristics and Molecular Mechanism. PLOS ONE 11(6): e0157700. https://doi.org/10.1371/journal.pone.0157700
[3] Xiaoren Tang and Salomon Amar. "Kavain inhibition of LPS-induced TNF-α via ERK/LITAF." Royal Society of Chemistry, Toxicol. Res., 2016, 5, 188-196
[4] Singh, Y. N., & Singh, N. N. (2002). Therapeutic Potential of Kava in the Treatment of Anxiety Disorders. CNS Drugs, 16(11), 731-743. doi:10.2165/00023210-200216110-00002
[5] Prinsloo, D., Dyk, S. V., Petzer, A., & Petzer, J. P. (2019). Monoamine Oxidase Inhibition by Kavalactones from Kava (Piper Methysticum). Planta Medica, 85(14/15), 1136-1142. doi:10.1055/a-1008-9491
[6] Schmidt N, Ferger B. Neuroprotective effects of (+/-)-kavain in the MPTP mouse model of Parkinson's disease. Synapse. 2001 Apr;40(1):47-54. doi: 10.1002/1098-2396(200104)40:1<47::AID-SYN1025>3.0.CO;2-S. PMID: 11170221.
