The results demonstrated that α-asarone effectively decreased the rise in neuroinflammatory response caused by LPS and inhibited the production of pro-inflammatory cytokines in BV-2 cells. Mechanistic investigations have demonstrated that α-Asarone reduces the activation of LPS stimulation by preventing the breakdown of the inhibitor kappa B-α signal in BV-2 microglia and regulating nuclear factor kappa-B [2].

The current findings show that an acute alpha-asarone therapy causes an immobile biphasic response. This means that at lower doses of alpha-asarone (15 and 20 mg/kg, i.p.), the duration of immobility is reduced, while at larger dosages, it increases. TST doses (i.p., 50 and 100 mg/kg). Furthermore, greater intraperitoneal injection doses of α-Asarone (50 and 100 mg/kg) markedly decreased spontaneous locomotor activity [1].

Interactions
The action of asarone and beta-asarone, alone or in combination with either reserpine or chloropromazine, on conditioned avoidance behavior in rats, fighting behavior in mice, and electroshock convulsions in rats was determined. ... Asarone potentiated the action of reserpine and chlorpromazine on conditioned avoidance behavior and fighting behavior; beta-asarone did not. ... Asarone potentiated the lethal effect of chlorpromazine during electroshock convulsions; beta-asarone did not. Pretreatment with Acorus oil, asarone, or beta-asarone did not increase the concentration of 5-hydroxytryptamine in rat brain. /Asarones/

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Non-Human Toxicity Values
LD50 Rat oral 1010 mg/kg bw /beta-Asarone/
LD50 Mouse oral 184.2 mg/kg bw /beta-asarone/
LD50 Mouse oral 418 mg/kg
LD50 Mouse ip 310 mg/kg

[1]. Biphasic Effects of α-Asarone on Immobility in the Tail Suspension Test: Evidence for the Involvement of the Noradrenergic and Serotonergic Systems in Its Antidepressant-Like Activity. Front Pharmacol. 2016; 7: 72.

[2]. α-Asarone attenuates microglia-mediated neuroinflammation by inhibiting NF kappa B activation and mitigates MPTP-induced behavioral deficits in a mouse model of Parkinson's disease. Neuropharmacology, Volume 97, October 2015, Pages 46–57.

[3]. Effect of α-asarone on angiogenesis and matrix metalloproteinase. Environmental Toxicology and Pharmacology, Volume 39, Issue 3, May 2015, Pages 1107–1114.

Alpha-asarone is the trans-isomer of asarone. It has a role as an anticonvulsant and a GABA modulator.
alpha-Asarone has been reported in Perilla frutescens, Asarum hypogynum, and other organisms with data available.
See also: beta-Asarone (annotation moved to).

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Mechanism of Action
Docking experiments using a number of published crystal structures of HMG-CoA reductase with the potent hypocholesterolemic agent alpha-asarone are described. The results indicate that alpha-asarone binds in the enzyme's active site. The methoxy groups play a key role in the binding and probably also in its biological activity, as shown by extensive SAR studies reported for analogues of alpha-asarone. The docking results will be valuable for the structure-based design of novel hypolipidemic agents.

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Therapeutic Uses
/EXPTL THER/ The results of the present report show that alpha-asarone was an inhibitor of hepatic HMG-CoA reductase and that the administration of alpha-asarone at 80 mg/kg bw for 8 days decreased serum cholesterol by 38% (p < 0.001) in hypercholesterolemic rats. This alpha-asarone treatment affected mainly the serum LDL-cholesterol levels, leaving serum HDL-cholesterol lipoproteins unaffected, with a consequent decrease of 74% in the LDL/HDL ratio. In addition, alpha-asarone especially stimulated bile flow in hypercholesterolemic rats (60%), increasing the secretion of bile salts, phospholipids and bile cholesterol. The drug also reduced the cholesterol levels of gallbladder bile, whereas the concentration of phospholipids and bile salts increased only slightly, leading to a decrease in the cholesterol saturation index (CSI) of bile in the hypercholesterolemic rats. This CSI decrease and the increase in bile flow induced by alpha-asarone may account for the cholelitholytic effect of alpha-asarone. It seems that alpha-asarone induced clearance of cholesterol from the bloodstream and that the excess of hepatic cholesterol provided by LDL-cholesterol is diverted to bile sterol secretion via a bile choleresis process. The inhibition of HMG-CoA reductase and the increase in bile flow induced by alpha-asarone, as well as the decrease in the CSI, could then explain the hypocholesterolemic and cholelitholytic effects of alpha-asarone.
/EXPTL THER/ After daily dosing po of 80 mg/kg of alpha-asarone ... for seven days to hypercholesterolemic male rats, cholesterol decreased 57.3% ... and triglycerides diminished 42.5% ..., respectively. ... alpha-asarone decreased 80.6% the weight of gallstones in hamsters. ... Alpha-asarone did not produce any toxic effect after oral administration to rats of 10 or 50 mg/kg for 28 days, or genotoxicity by the dominant lethal test. ... No teratogenicity was observed in pregnant rats during organogenesis but in mice slight fetal toxicity was manifested by hydrocephaly, skeletal defects and fetal weight retardation ...
/EXPTL THER/ There was no significant difference between the antifungal activity of beta and alpha-asarone in crude drugs.

C12H16O3

208.2536

208.109

2883-98-9

636822

White to off-white solid powder

1.0±0.1 g/cm3

296.0±0.0 °C at 760 mmHg

57-61 °C(lit.)

107.7±23.8 °C

0.0±0.6 mmHg at 25°C

1.526

2.98

0

3

4

15

203

0

C/C=C/C1=CC(=C(C=C1OC)OC)OC

RKFAZBXYICVSKP-AATRIKPKSA-N

InChI=1S/C12H16O3/c1-5-6-9-7-11(14-3)12(15-4)8-10(9)13-2/h5-8H,1-4H3/b6-5+

1,2,4-trimethoxy-5-[(E)-prop-1-enyl]benzene

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~480.19 mM)
H2O : ~0.67 mg/mL (~3.22 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (12.00 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (12.00 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (12.00 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)