α-Santalol
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α-Santalol (cis-α-Santalol), a naturally occurring sesquiterpene, is an orally active anticancer agent and apoptosis inducer. α-Santalol activates caspase-3 to drive apoptotic processes. >α-Santalol induces apoptosis, decreases cell viability, and causes PARP cleavage in human prostate cancer cells. α-santalol inhibits Akt/Survivin pathway to induce cell death. α-Santalol can be used for the research of prostate cancer and diabetes mellitus.
For research use only. We do not sell to patients.
- Purity: 97.62%
- CAS No.: 115-71-9
- Formula: C15H24O
- Molecular Weight:220.35
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Storage:
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
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Biological Activity
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Caspase 3 |
α-Santalol (25-75 μM; 24-48 h) decreases viability of androgen-independent PC-3 and androgen-dependent LNCaP human prostate cancer cells in a concentration- and time-dependent manner with an IC50 < 50 μM, while normal human prostate epithelial PrEC cells are relatively resistant to its growth-suppressive effects[1].
α-Santalol (25-50 μM; 24 h) induces apoptotic DNA fragmentation in human prostate cancer PC-3 and LNCaP cells, with LNCaP cells showing greater sensitivity to this effect than PC-3 cells[1].
α-Santalol (50 μM; 24 h) induces morphological features of apoptosis, including condensed and fragmented nuclear DNA, in human prostate cancer PC-3 and LNCaP cells[1].
α-Santalol (50 μM; 24 h) activates caspase-3 in human prostate cancer PC-3 and LNCaP cells, with a more robust response observed in LNCaP cells[1].
α-Santalol (25-50 μM; 24-48 h) induces cleavage of PARP, a downstream substrate of active caspase-3, in human prostate cancer LNCaP cells[1].
α-santalol (20, 40 μM) resulted in the down regulation of survivin and p-AKT (s-473) expression and statistically significant reduction in total survivin levels in prostate cancer cells[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:PC-3 cells, LNCaP cells, PrEC cells
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Concentration:25 μM, 50 μM, 75 μM
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Incubation Time:24 h, 48 h
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Result:Decreased PC-3 cell viability by ~75% after 24-h treatment with 50 μM.
Showed greater growth inhibition sensitivity in LNCaP cells than in PC-3 cells at 48 h.
Reduced PrEC cell viability by ~44% with 75 μM for 24 h, with minimal effects at 25 and 50 μM.
Achieved an IC50 < 50 μM in prostate cancer cells.
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Cell Line:PC-3 cells, LNCaP cells
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Concentration:25 μM, 50 μM
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Incubation Time:24 h
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Result:Increased cytoplasmic histone-associated DNA fragmentation statistically significantly in both PC-3 and LNCaP cells after 24-h treatment with 50 μM, with an enrichment factor of ~3 in PC-3 cells and ~6 in LNCaP cells.
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Cell Line:PC-3 cells, LNCaP cells
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Concentration:50 μM
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Incubation Time:24 h
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Result:Increased the percentage of apoptotic cells with condensed/fragmented DNA statistically significantly after 24-h treatment, which were rarely observed in control cultures.
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Cell Line:LNCaP cells
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Concentration:25 μM, 50 μM
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Incubation Time:24-48 h
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Result:Induced strong expression of cleaved 89 kDa PARP in LNCaP cell lysates.
Increased expression of cleaved 89 kDa PARP at 48 h compared to 24 h.
α-Santalol (12.5-200 mg/kg; 100-200 μg/10 μL; i.p.; p.o.; i.c.v.; single dose) dose-dependently induces central nervous system depressant effects in male ddY mice, including up to 95% reduction in spontaneous locomotor activity at 50 mg/kg i.p., 95% inhibition of acetic acid-induced writhing at 50 mg/kg i.p., and significant increases in hexobarbital-induced sleeping time, hypothermia, and brain HVA/5-HIAA levels at higher doses[2].
α-Santalol (100 mg/kg BW; i.p.) reduces blood glucose by 61% and modulates associated physiological and biochemical parameters to normoglycemic levels in Alloxan (HY-W017227)-induced diabetic male Swiss albino mice[3].
α-Santalol (100 mg/kg BW; i.p.) increases body weight by 27.75% and modulates key oxidative stress and liver function parameters in d-galactose-induced oxidative stress male Swiss albino mice[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:ddY mice (male, 23-30 g, 8 per group)[2]
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Dosage:12.5-50 mg/kg (i.p.); 25-200 mg/kg (p.o.); 100-200 μg/10 μl (i.c.v.)
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Administration:i.p.; p.o.; i.c.v.; single dose
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Result:Increased hexobarbital-induced sleeping time .
Reduced acetic acid-induced writhing number.
Reduced Methamphetamine-induced locomotor activity across all intervals.
Increased brain homovanillic acid (HVA) levels to 171% of control.
Produced no significant effect on Reserpine-induced hypothermia.
Produced no significant anticonvulsant effects in chemically-induced or electroshock-induced seizure models (50 mg/kg i.p. and 200 mg/kg p.o.).
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Animal Model:Swiss albino (male, adult 4 months old, 20-30 g, alloxan-induced diabetic)[3]
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Dosage:100 mg/kg BW
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Administration:i.p.
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Result:Increased body weight by 8.1%.
Reduced water consumption by 89%.
Reduced serum bilirubin by 42.9%.
Reduced serum malondialdehyde (MDA) by 46.1%.
Reduced liver weight by 36.3%.
Increased liver glycogen by 87.4%.
Increased total liver protein by 23.5%.
Reduced blood glucose levels by 61% over 8 days, returning blood glucose to normoglycemic levels (93 ± 9 mg/dl on Day 8).
Chemical Information
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CAS No. 115-71-9
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Appearance Liquid (Density: 0.977 g/cm3)
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Molecular Weight 220.35
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Formula C15H24O
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Color Colorless to light yellow
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SMILES
CC12C(C3)[C@@H]1CC3[C@](C)2CC/C=C(C)\CO
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Synonyms
cis-α-Santalol
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
-20°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Purity & Documentation
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Data Sheet (278 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Portuguese - PT (393 KB)
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Handling Instructions (2659 KB)
References
[1]. Bommareddy A, et al. α-Santalol, a derivative of sandalwood oil, induces apoptosis in human prostate cancer cells by causing caspase-3 activation. Phytomedicine. 2012;19(8-9):804-811. [Content Brief]
[2]. Okugawa H, et al. Effect of α-santalol and β-santalol from sandalwood on the central nervous system in mice. Phytomedicine. 1995;2(2):119-126. [Content Brief]
[3]. Misra BB, et al. Evaluation of in vivo anti-hyperglycemic and antioxidant potentials of α-santalol and sandalwood oil. Phytomedicine. 2013;20(5):409-416. [Content Brief]
[4]. Bommareddy A, McGlynn D, Lewis M, Lockus L, Seward J, Hong KL, VanWert AL, Dwivedi C. Akt/survivin pathway inhibition enhances the apoptotic cell death-induced by alpha-santalol in human prostate cancer cells. Fitoterapia. 2020 Jun;143:104552. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
α-Santalol Related Classifications
Cat. No.: HY-N11908
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- α-Santalol
- 115-71-9
- cis-α-Santalol
- Akt
- Survivin
- Apoptosis
- Caspase
- PARP
- caspase-3
- alloxan-induced diabetic male Swiss albino mice
- mouse brain
- normal human prostate epithelial PrEC cells
- d-galactose-mediated oxidative stress-induced male Swiss albino mice
- human prostate cancer PC-3 cells
- human prostate cancer cells
- human prostate cancer LNCaP cells
- skin cancers
- Inhibitor
- inhibitor
- inhibit