| Identification | Back Directory | [Name]
A-SPINASTEROL | [CAS]
481-18-5 | [Synonyms]
α
-amine D2
BESSISTEROL
spinasterol
Hitdesterol
Benzyl-α
HITODESTEROL
A-SPINASTEROL
Α-SPINASTEROL
SPINASTEROL, A-
alpha-Spinastero
ALPHA-SPINASTEROL
alpha-spinasterin
DELTA7-STIGMASTEROL
A-SPINASTEROL USP/EP/BP
(24R)-5α-Stigmasta-7,22-dien-3β-ol
(22E)-5α-Stigmasta-7,22-dien-3β-ol
(3β,5α,22E)-Stigmasta-7.22-dien-3-ol
Stigmasta-7,22-dien-3-ol, (3β,5α,22E)-
(e)-5-alpha-stigmasta-22-dien-3-beta-ol
(3-beta,5-alpha,22e)-stigmasta-22-dien-3-ol
5-alpha-Stigmasta-7,22-dien-3-beta-ol, (E)-
(3-beta,5-alpha,22e)-stigmasta-7,22-dien-3-ol
7,22,5ALPHA-CHOLESTADIEN-24BETA-ETHYL-3BETA-OL
(3S,5S,9R,10S,13R,14R,17R)-17-[(E,2R,5S)-5-ethyl-6-methylhept-3-en-2-yl]-10,13-dimethyl-2,3,4,5,6,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol | [EINECS(EC#)]
200-258-5 | [Molecular Formula]
C29H48O | [MDL Number]
MFCD00200554 | [MOL File]
481-18-5.mol | [Molecular Weight]
412.69 |
| Chemical Properties | Back Directory | [Melting point ]
168-169° | [alpha ]
D25 -3.6° (c = 2.8 in chloroform) | [Boiling point ]
500.0±44.0 °C(Predicted) | [density ]
0.98±0.1 g/cm3(Predicted) | [storage temp. ]
2-8°C | [solubility ]
Chloroform (Slightly), Ethyl Acetate (Slightly, Heated), Methanol (Slightly, Heated) | [form ]
Solid | [pka]
15.10±0.70(Predicted) | [color ]
White to Off-White | [biological source]
Aster scaber | [Stability:]
Light Sensitive |
| Hazard Information | Back Directory | [Uses]
α-Spinasterol was identified as a novel transient receptor potential vanilloid 1 antagonist with antinociceptive properties. | [Definition]
ChEBI: Alpha-Spinasterol is a steroid. It derives from a hydride of a stigmastane. | [Biological Activity]
α-Spinasterol is a blood-brain barrier-permeable and orally active plant phytosterol with antioxidantanticonvulsant (0.1-1 mg/kg i.p. in mice)antidepressant (1-2 mg/kg i.p. in mice) and anti-inflammatory (0.001-1 mg/kgi.p. or 1-10 mg/kgi.g. in mice) propertiesas well as antinociceptive efficacy via dual actions against transient receptor potential vanilloid 1 (TrpV1; IC50/Emax = 1.4 μM/67% against 2 nM RTX for binding mouse spinal cord membranes; IC50/Emax = 40 μM/62% against 20 μM capsaicin-induced mouse spinal cord synaptosomes Ca2+ influx) and cyclooxygenases (IC50 = 16.17 μM/COX1 and 7.76μM/COX2). a-spinasterol can directly affect membrane structure and packing in a manner similar to cholesterolboth a-spinasterol and stitosterol are reported to lower plasma/liver cholesterol levels and increase fecal cholesterol excretion when supplemented in daily diet (1%) in mice in vivo.''α-Spinasterol is a constituent of argan oi | [in vivo]
α-Spinasterol (0.5-2.5 mg/kg, oral, 6 weeks) lowers serum triglycerides in mice and improves symptoms of diabetes[2].
α-Spinasterol (0.1-1 mg/kg, oral, 24 h) has anti-nociceptive effects in postoperative and neuropathic pain models in mice[3].
α-Spinasterol (0-2 mg/kg, i.p., single dose) exhibits antidepressant effects in mice but does not show anxiolytic effects[4].
α-Spinasterol (0.001-10 mg/kg, i.g., single dose) significantly reduces inflammatory cell infiltration induced by LPS (HY-D1056) in mice[5].
α-Spinasterol (0.001-1 mg/kg, i.p., single dose) can inhibit leukocytes and mononuclear cells in mice, with ID50 at 0.006 (0.002-0.01) mg/kg and 0.004 (0.002-0.007) mg/kg[5].
α-Spinasterol (0.001-1 mg/kg, i.p., single dose) has anticonvulsant activity in mice without affecting their neuromuscular strength, impairing motor coordination, or changing body temperature[6]. | Animal Model: | Streptozotocin-induced diabetic mice[2] | | Dosage: | 0.5 and 2.5 mg/kg/day; 6 weeks | | Administration: | Oral | | Result: | Reduced serum triglycerides in mice, kidney weight, and urinary protein excretion, without affecting serum glucose levels. |
| Animal Model: | Mouse postoperative pain models (surgery incision induced) or different neuropathic pain models (trauma or chemotherapy induced)[3] | | Dosage: | 0.1, 0.3, 1 mg/kg; 24 h | | Administration: | Oral | | Result: | Relieved post-operative pain, reduce cell infiltration in damaged tissues, alleviated some mechanical ectopic pain caused by sciatic nerve ligation and mechanical and cold ectopic pain induced by paclitaxel, without altering spontaneous or forced motor activity, causing gastric damage, or leading to changes in the liver and kidneys, and without affecting the cell viability in mouse cortical and spinal cord slices.
Inhibited COX-1 and COX-2 enzyme activity without altering the animal's body temperature. |
| Animal Model: | Na?ve male Albino Swiss mice[4] | | Dosage: | 0, 0.5, 1, 2 mg/kg; 0.5-2 mg/kg; single dose | | Administration: | Intraperitoneal injection (i.p.) | | Result: | Showed an anti-immobility effect in the forced swimming test on mice, with no significant changes in body temperature and no alteration in the mice's spontaneous movement activity. Showed no anti-anxiety effects in the elevated plus maze and light-dark box tests. |
| Animal Model: | LPS(HY-D1056)-induced peritonitis in mice[5] | | Dosage: | 0.001-1 mg/kg; 1-10 mg/kg; single dose | | Administration: | i.g. | | Result: | Reduced inflammatory cell infiltration in LPS-injected mice. |
| Animal Model: | Mice induced by PTZ ;Mice induced by 6 Hz [6] | | Dosage: | 0, 0.02, 0.1, 0.5, 1 mg/kg; single dose | | Administration: | Intraperitoneal injection (i.p.) | | Result: | Showed higher doses of 0.5 and 1 mg/kg significantly increased the threshold for chronic seizures without affecting the sensitivity of mice to the forelimb rigidity induced by PTZ. The CS50 values in the 0.5 mg/kg and 1 mg/kg groups were significantly increased. Did not affect the neuromuscular strength of the mice, did not impair motor coordination, and did not change the body temperature. |
| [target]
TRPV | HMG-CoA reductase | [IC 50]
COX-1: 16.17 μM (IC50); COX-2: 7.76 μM (IC50); TRPV1 | [storage]
4°C, protect from light |
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