+86-28-82633987
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.
HPLC of Dihydrokawain
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
35.5300
2.9992
2.9991
.1797
4.0022
14.8481
High
87.6789
2.8099
Yes
Yes
No
No
No
No
0.0
No
Yes
Yes
Yes
Dihydrokawain (CAS No.: 587-63-3) is a naturally occurring aromatic ether compound, classified as a 2-pyranone compound. As one of the main active ingredients in the Piper methysticum plant, dihydrodrunicapacin has attracted widespread attention in recent years due to its remarkable bioactivity, especially its potential for anti-inflammatory applications. Inflammatory responses are a key link in the occurrence and development of various chronic diseases, and the development of natural product drugs targeting inflammation-related targets has become an important direction in current pharmacological research. This paper aims to systematically review the chemical structure and physicochemical properties of dihydrodrunicapacin, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, pharmacokinetic characteristics, and clinical application prospects, aiming to provide a theoretical foundation and research direction for future drug development of dihydrodunciol.
The molecular formula of dihydrodrunkedoshanin is C14H16O3, with a molecular weight of 232.2790. Its structural core is a 2-pyranone ring attached to an aromatic ether group, and the overall molecule exhibits moderate lipid solubility (LogP=2.9992), indicating good membrane permeability. The polar surface area (TPSA) was 35.53 Ų, indicating that its molecular polarity is relatively low, which facilitates membrane penetration. Low water solubility (0.1797 mg/mL) suggests limited solubility in the aqueous phase but suitable for lipid media environments.
From a safety perspective, dihydrodrunokitazin did not show hERG channel inhibitory effects, reducing the risk of cardiotoxicity; The Ames test result was 0.0, indicating no significant mutagenicity. Additionally, this compound has a high blood-brain barrier penetration ability, suggesting its potential to act in the central nervous system.
Dihydrodrunicapitol is mainly found in the traditional medicinal plant of the Pacific region—Piper methysticum. Kava is a perennial shrub whose roots are rich in active ingredients and have traditionally been used to make soothing, anti-anxiety, and anti-inflammatory beverages. Dihydrodrunicaphanol, as one of the main 2-pyranone compounds in kava, has its content and extraction purity directly affect the efficacy of kava products.
Common methods for extracting dihydrodrunicaphanin include solvent extraction, liquid-liquid distribution, and column chromatography purification. Ethanol or methanol is generally used as extraction solvents, and efficiency is improved through ultrasound-assisted extraction or reflux extraction. Subsequently, silica gel column chromatography or high-performance liquid chromatography (HPLC) were used for separation and purification, ultimately yielding high-purity dihydrodruniophysin. In recent years, supercritical CO2 extraction technology has also been applied to extract dihydrodruniospicin in Kava, offering advantages of environmental friendliness and high efficiency.
The anti-inflammatory effect of dihydrodrunicaphanin is one of its most notable pharmacological activities. Multiple in vitro and in vivo experiments have shown that dihydroduphimol can significantly inhibit the production of inflammatory mediators and the activation of inflammatory signaling pathways. Its main manifestation is inhibiting the expression of pro-inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-6 (IL-6), while reducing cyclooxygenase (PTGS1 and PTGS2) activity, thereby decreasing prostaglandin synthesis.
Additionally, dihydrodruniocaphanin can regulate the inflammation-related transcription factor NF-κB (NFKB1) and signal transduction and transcription activator factor 3 (STAT3), inhibiting their intranuclear translocation and gene transcription activity, thereby reducing inflammatory responses. Its regulatory effect on the inflammasome component CASP1 has also been reported, suggesting it may reduce the release of the pro-inflammatory cytokine IL-1β by inhibiting inflammasome activation.
Because dihydrodrunicaphanol has high blood-brain barrier permeability, its pharmacological effects in the central nervous system are gradually being revealed. Research shows that dihydrodrunctitol can regulate TRPV1 and TRPA1, two ion channels closely related to pain perception, exhibiting analgesic and neuroprotective effects. By regulating the activity of these channels, dihydrodruniophorin reduces neuroinflammation and pain signal transmission, offering potential value in treating neuropathic pain.
Some studies have also found that dihydrodruniophysine has antioxidant activity, can scavenge free radicals, and reduce cellular damage caused by oxidative stress. Additionally, its regulatory effect on nitric oxide synthase 2 (NOS2) suggests its potential role in regulating immune responses and vascular function.
The anti-inflammatory and analgesic effects of dihydrodrunctitol are mainly achieved through multi-target and multi-pathway coordinated regulation. Key targets include:
IL-6 and TNF: As pro-inflammatory cytokines, IL-6 and TNF play central roles in inflammatory responses. Dihydrodruniospicyl reduces inflammatory responses by inhibiting its expression and secretion.
STAT3 and NFKB1: These two transcription factors are key nodes in inflammatory signaling. Dihydrodrunioscaphin can inhibit its activation and block the transcription of inflammation-related genes.
CASP1: The core component of the inflammasome, involved in the maturation and release of IL-1β. Dihydrodruniospicyl inhibition of CASP1 reduces the release of pro-inflammatory cytokines.
TRPV1 and TRPA1: These two ion channels are involved in pain and inflammation signaling. Dihydrodrunkyanin exerts analgesic and anti-inflammatory effects by modulating its activity.
PTGS1 and PTGS2: cyclooxygenase enzymes that catalyze prostaglandin synthesis. Dihydrodrunokitachin inhibits its activity and reduces the formation of inflammatory mediators.
NOS2: Induced nitric oxide synthase, involved in inflammation and immune responses. Dihydrodruniospicol regulates NOS2 expression and reduces inflammatory damage.
In summary, dihydrodrunkonin synergistically regulates inflammatory signaling pathways through multiple targets, exerting significant anti-inflammatory and analgesic effects.
The druggability parameters of dihydro duptophyllamine indicate its promising potential for drug development. The molecular weight is moderate, with a LogP value close to 3, meeting the Lipinski rule and facilitating oral absorption. Its relatively low polar surface area and moderate water solubility support its good distribution in the body. High blood-brain barrier permeability makes central nervous system applications possible.
In terms of safety, dihydrodruniosamine does not inhibit hERG channels or pose a risk of mutagenicity, reducing concerns about cardiotoxicity and genotoxicity. Preliminary pharmacokinetic studies indicate that dihydrodrunicapitol has good bioavailability and distribution characteristics in the body, but its metabolic pathways and excretion mechanisms still require further study.
Additionally, dihydrodruniospicyl has relatively low water solubility, which may affect the bioavailability of oral formulations. Therefore, future drug formulation development should consider strategies to improve solubility, such as nanocarriers and solid dispersions.
Based on the significant activity of dihydrodrunk drunk in anti-inflammatory, analgesic, and neuroprotective effects, its application prospects in various inflammation-related diseases are broad. In chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and neuropathic pain, dihydrodruniophyllain is expected to become a candidate for new natural medicines.
Furthermore, considering its good blood-brain barrier permeability, the potential protective effect of dihydrodrunicaphanin in neurodegenerative diseases such as Alzheimer's and Parkinson's is worth further exploration. Future research should strengthen in vivo pharmacokinetics, toxicological evaluation, and mechanistic studies to promote clinical translation.
By integrating modern drug formulation technologies and optimizing the properties of dihydrodrunicaphanin, improving its bioavailability and targeting will further promote its clinical application development. The multi-target mechanism of action also provides a theoretical basis for combination drug strategies, helping to improve treatment outcomes and reduce side effects.
Dihydrodrunicaphanol, a 2-pyranone aromatic ether compound derived from the traditional medicinal plant kava, demonstrates significant anti-inflammatory, analgesic, and neuroprotective effects. Its multi-target and multi-pathway mechanism of action provides a valuable example for pharmacological research of natural products. Good druggability parameters and safety evaluation have laid the foundation for its drug development.
In the future, by integrating modern medicinal chemistry, pharmacology, and formulation technologies, in-depth elucidation of the mechanism of action and in vivo metabolic characteristics of dihydrodrunicapitol will help promote its clinical application and meet new demands in the treatment of inflammatory and neurological diseases. Dihydrodrunuijian is undoubtedly a star compound worth looking forward to in the field of natural product pharmacology.
Shenshuai
Wenjing
Hedandan
