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Dihydrokawain

CAS No.:587-63-3

Dihydrokawain
Catalogue No.: BP0495
Formula: C14H16O3
Mol Weight: 232.279
Botanical Source: Piper methysticum Forst
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Dihydrokawain

CAS No.:587-63-3

Dihydrokawain
Catalogue No.: BP0495
Formula: C14H16O3
Mol Weight: 232.279
Botanical Source: Piper methysticum Forst
Contacts
+86-28-82633860  +86-18080483897
 
Email: sales@biopurify.com biopurify@gmail.com
Over 15 years of industry experience in phytochemicals from R&D(reference substances) to Industrialization, please feel free to contact us!

Synonym name: Marindinin
Catalogue No.: BP0495
Cas No.: 587-63-3
Formula: C14H16O3
Mol Weight: 232.279
Botanical Source: Root of Piper methysticum and Aniba gigantifolia

Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams.

For Reference Standard and R&D, Not for Human Use Directly.
Inquire for bulk scale.

 

 

Description:

Dihydrokavain may play an important role in regulation of GABAergic neurotransmission, it non-competitively inhibits the specific binding of [3H]-batrachotoxinin-A 20-alpha-benzoate to receptor site 2 of voltage-gated Na+ channels. Dihydrokavain may treat sleep disturbances, as well as stress and anxiety.

 

References:

Planta Med. 2002 Dec;68(12):1092-6.    

Kavalactones and dihydrokavain modulate GABAergic activity in a rat gastric-brainstem preparation.

METHODS AND RESULTS:

Using an in vitro neonatal rat gastric-brainstem preparation, the activity of majority neurons recorded in the nucleus tractus solitarius (NTS) of the brainstem were significantly inhibited by GABA A receptor agonist, muscimol (30 microM), and this inhibition was reversed by selective GABA A receptor antagonist, bicuculline (10 microM). 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 %. 

CONCLUSIONS:

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.