|Source:||The roots of Piper methysticum Forst|
|Biological Activity or Inhibitors:||1. Dihydrokavain may play an important role in regulation of GABAergic neurotransmission.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||4.3053 mL||21.5267 mL||43.0533 mL||86.1067 mL||107.6334 mL|
|5 mM||0.8611 mL||4.3053 mL||8.6107 mL||17.2213 mL||21.5267 mL|
|10 mM||0.4305 mL||2.1527 mL||4.3053 mL||8.6107 mL||10.7633 mL|
|50 mM||0.0861 mL||0.4305 mL||0.8611 mL||1.7221 mL||2.1527 mL|
|100 mM||0.0431 mL||0.2153 mL||0.4305 mL||0.8611 mL||1.0763 mL|
Planta Med. 2002 Dec;68(12):1092-6.
|Kavalactones and dihydrokavain modulate GABAergic activity in a rat gastric-brainstem preparation.[Pubmed: 12494336]|
|Application of kavalactones (300 microg/ml) and Dihydrokavain (300 microM) into the brainstem compartment of the preparation also significantly reduced the discharge rate of these NTS neurons (39 % and 32 %, respectively, compared to the control level), and this reduction was partially reversed by bicuculline (10 microM). Kavalactones or Dihydrokavain induced inhibitory effects were not reduced after co-application of saclofen (10 microM; a selective GABA B receptor antagonist) or naloxone (100 nM; an opioid receptor antagonist). Pretreatment with kavalactones (300 microg/ml) or Dihydrokavain (300 microM) significantly decreased the NTS inhibitory effects induced by muscimol (30 microM), approximately from 51 % to 36 %. Our results demonstrated modulation of brainstem GABAergic mechanism by kavalactones and Dihydrokavain, and suggested that these compounds may play an important role in regulation of GABAergic neurotransmission.|
Planta Med. 1998 Jun;64(5):458-9.
|Kavain, dihydrokavain, and dihydromethysticin non-competitively inhibit the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels.[Pubmed: 9690349]|
|The mode of action of the kava pyrones, kavain, Dihydrokavain and dihydromethysticin on the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to epitope 2 of voltage-dependent Na+ channels was investigated by performing saturation experiments in the presence and absence of these kava pyrones. The tested compounds significantly decreased the apparent total number of binding sites (Bmax) for [3H]-batrachotoxinin-A 20-alpha-benzoate (control: 0.5 pmol/mg protein, kava pyrones: 0.2-0.27 pmol/mg protein) with little change in the equilibrium constants (KD) for [3H]-batrachotoxin-A 20-alpha-benzoate (control: 28.2 nM, kava pyrones: 24-31 nM). The results indicate for the kava pyrones a non-competitive inhibition of the specific [3H]-batrachotoxinin-A 20-alpha-benzoate binding to receptor site 2 of voltage-gated Na+ channels.|