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Synonym name: Betulanonaprenol; Nonaisoprenol; Betulaprenol
Catalogue No.: BP1321
Cas No.: 13190-97-1
Formula: C45H74O
Mol Weight: 631.086
Botanical Source: Also from Nicotiana tabacum (tobacco)
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.
HPLC of Solanesol
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
20.2300
12.9236
12.9236
.0000
5.3875
3.6872
High
98.3687
3.1993
Yes
Yes
Yes
No
No
No
0.0
No
Yes
Yes
Yes
Solanesol (CAS No.: 13190-97-1) is a naturally occurring aliphatic terpene alcohol, mainly distributed among Solanaceae plants, with tobacco (Nicotiana tabacum) being the primary source. As an orally active compound, antanisol has gradually become a hot topic in natural product pharmacology research in recent years due to its diverse biological activities and potential medicinal value. Its remarkable antioxidant, anti-inflammatory, and neuroprotective effects have given it broad application prospects in fields such as neurodegenerative diseases, chronic inflammation, and metabolic disorders. This paper will systematically review the chemical structure and physicochemical properties of ketanyol, plant origin and extraction process, pharmacological activity and mechanism of action, druggability evaluation, pharmacokinetic characteristics, and, combined with current preclinical research findings, explore its future clinical application potential.
Ketaniol is a long-chain aliphatic terpene alcohol with the molecular formula C45H74O and a molecular weight of 631.0860. Its structure consists of nine isoprene units connected by a head-to-tail mechanism, making it a non-cyclic polyterpenoid compound. The structural characteristics of cyclanisol are characterized by high hydrophobicity, with a LogP value as high as 12.9236, indicating its strong lipid solubility. Its extremely low polar surface area (TPSA of 20.23) and water solubility (almost zero) indicate that its solubility in the aqueous phase is extremely low, but it possesses strong cell membrane penetration capability.
The molecular structure of cyclanisol contains multiple double bonds and hydroxyl groups, giving it certain chemical reactivity and playing an important role in antioxidant reactions. Its high lipid solubility and good blood-brain barrier permeability (BBB high permeability) give it potential advantages in treating central nervous system diseases. Additionally, cyclanisol does not exhibit hERG channel inhibitory activity, and the Ames mutagenicity test results are negative, indicating good safety and a solid foundation for druggability.
Cyclanisol is mainly found in Solanaceae plants, especially abundant in tobacco leaves, with concentrations reaching 3%-5%. Additionally, antlanyl is found in the leaves and stems of tomatoes, eggplants, and chili peppers, but in relatively low amounts. Tobacco, as the main industrial source of cyclanisol, has become the preferred plant resource for extracting enenylinol due to its short growth cycle and high yield.
The main methods for extracting oclaninol include solvent extraction, supercritical CO2 extraction, and membrane separation technology. Traditional solvent extraction typically uses organic solvents such as ethanol and hexane, obtained by extraction and concentration to obtain crude extracts, followed by purification by silica gel column chromatography or high-performance liquid chromatography (HPLC). Supercritical CO2 extraction technology, due to its environmental friendliness, absence of solvent residues, and strong selectivity, has been widely used in recent years for the extraction of lanitol, effectively improving extraction rate and purity. In addition, the combination of membrane separation technology with extraction processes helps achieve large-scale production and purification of cyclanisol.
Cyclanisol possesses a variety of biological activities, including antioxidant, anti-inflammatory, neuroprotection, anti-apoptotic effects, and lipid-regulating properties, demonstrating broad pharmacological potential.
Cyclanisol can significantly induce the expression of intracellular antioxidant enzymes such as heme oxygenase-1 (HO-1) and heat shock protein 70 (Hsp70), thereby enhancing the cells' antioxidant defense capabilities. By activating the p38 MAPK and Akt signaling pathways, it regulates oxidative stress responses, reduces the production of reactive oxygen species (ROS), and protects cells from oxidative damage.
Inflammatory responses are the core pathological processes of many chronic diseases. Ketanisol demonstrates significant anti-inflammatory effects by inhibiting the release of pro-inflammatory factors and activating signaling pathways. Research shows that cyclanisol can downregulate the NF-κB pathway, reducing the expression of inflammatory mediators such as TNF-α and IL-1β, thereby alleviating chronic inflammatory states.
Cyclanisol exhibits neuroprotective effects in various models of neurodegenerative diseases. It slows the progression of nerve damage by inhibiting neuronal apoptosis (reducing the cleavage of caspase-3 and PARP), alleviating oxidative stress and inflammatory responses. Related studies have shown that cyclanisol has potential therapeutic value for diseases such as Huntington's disease, Alzheimer's disease, and bipolar disorder.
Ketanisol inhibits the activation of apoptosis-related proteins by activating cell survival signaling pathways (such as Akt), reducing the levels of caspase-3 and PARPM cleavage, thereby protecting cells from programmed death. This mechanism plays an important role in protecting various tissues and preventing and treating diseases.
Cyclanisol has shown positive effects in regulating lipid metabolism. Its targets include cholesterol ester transfer protein (CETP), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), proproprotein convertase lysosozyme 9 (PCSK9), apolipoprotein E (APOE), and peroxisome proliferator-activated receptor α (PPARA). By modulating these targets, cyclanisol helps lower plasma cholesterol and triglyceride levels, improving dyslipidemia.
The multiple pharmacological effects of cyclanisol are attributed to its regulation of multiple cellular signaling pathways and key molecules.
Cyclaninol significantly induced the expression of antioxidant defense enzyme HO-1 and cell protection protein Hsp70. As an important enzyme in cellular stress responses, HO-1 can break down heme into antioxidant products, reducing oxidative damage. Hsp70 enhances cell resistance to stress by stabilizing protein structures and preventing misfolding.
Cyclanisol activates the p38 MAPK signaling pathway, promoting cellular adaptive responses to oxidative stress. At the same time, activation of the Akt pathway promotes cell survival and metabolic regulation, suppresses apoptosis signals, and maintains cellular homeostasis. The synergistic effect of these two pathways is key to the antioxidant and anti-apoptotic effects of cyclanisol.
By inhibiting the cleavage of caspase-3 and PARP, cyclanisol blocks the execution phase of apoptosis, protecting cells from damage caused by programmed death. This mechanism is especially important in neuroprotection and liver protection.
Cyclanisol affects cholesterol synthesis, transport, and metabolism by regulating key targets such as CETP, HMGCR, LDLR, APOB, PCSK9, APOE, and PPARA. For example, inhibiting HMGCR activity reduces cholesterol synthesis, activating LDLR to promote cholesterol clearance, and regulating PCSK9 to reduce LDL receptor degradation, thereby overall regulation of blood lipid levels.
Druggability evaluation of cyclanisol shows good safety and drug compatibility. Its high lipid solubility and extremely low water solubility determine its distribution in the body, especially its ability to effectively cross the blood-brain barrier, making it suitable for treating central nervous system diseases. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity; Ames test results showed no mutagenicity and relatively high safety.
However, the high LogP value of cyclanisol also presents challenges in bioavailability and solubility, limiting its oral absorption efficiency. To overcome this issue, researchers have attempted to improve its solubility and bioavailability through pharmaceutical strategies such as nanocarriers, liposome encapsulation, and solid dispersions.
Currently, pharmacokinetic studies of cyclanisol show that it has a relatively long half-life in the body, mainly metabolized by the liver, and partially excreted through bile. Its plasma protein binding rate is relatively high, indicating widespread distribution in the body, especially significant accumulation in adipose and brain tissue.
Due to its multi-target and multi-mechanism pharmacological activity, Ketanisol demonstrates broad application potential in various disease treatment fields.
Cyclanisol demonstrates neuroprotective and anti-inflammatory effects in neurodegenerative diseases such as Alzheimer's, Huntington's disease, and bipolar disorder, helping to slow disease progression and improve neurological dysfunction. Its excellent blood-brain barrier penetration provides important advantages for central nervous system drug development.
Ketanisol has protective effects against alcoholic liver disease, reducing liver cell damage through antioxidant and anti-inflammatory mechanisms, promoting liver function recovery, and has potential liver-protective value.
Ketanyol regulates inflammatory factors and signaling pathways to relieve chronic inflammatory pain, making it a potential adjunct treatment option for chronic pain syndrome.
In animal models of anxiety disorders and bipolar disorder, cyclanisol has shown certain anti-anxiety and emotionally stabilizing effects, suggesting its potential application in the treatment of mental illnesses.
By modulating various lipid metabolism-related targets, cyclanisol is expected to become a new lipid-lowering drug, helping to control dyslipidemia and prevent atherosclerosis and cardiovascular events.
Although clinical research on cyclanisol is still in its early stages, future efforts will need to strengthen its pharmacokinetics, toxicology, and clinical trial systems, optimize formulations and administration regimens, and promote clinical translation.
Cyclanisol, a natural aliphatic terpene alcohol with multiple biological activities, has become a research hotspot in the field of natural product pharmacology due to its remarkable antioxidant, anti-inflammatory, neuroprotective, and lipid-regulating effects. Its unique chemical structure and excellent blood-brain barrier penetration give it broad application prospects in neurodegenerative and metabolic diseases. Despite challenges such as poor water solubility and low bioavailability, the development of modern pharmaceutics technology provides strong support for the clinical application of cyclanisol. In the future, by thoroughly exploring its mechanism of action, optimizing formulation technology, and conducting systematic clinical evaluations, Cyclanisol is expected to become a novel natural drug for treating various diseases and driving innovative development in natural product pharmacology.
Shenshuai
Wenjing
Hedandan
