Synonym name:
Catalogue No.: BP0460
Cas No.: 30045-16-0
Formula: C22H24NO4+
Mol Weight: 366.436
Botanical Source: Quaternary alkaloid from Corydalis ambigua and several other Corydalis spp. and from Berberis floribunda (Fumariaceae, Berberidaceae)
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:
Dehydrocorydalin has anti-inflammatory,antinociceptive,antiplatelet,and anti-tumor effects and can protect the cardiovascular system. Dehydrocorydaline stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. Dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.
References:
Phytother Res. 2017 Mar;31(3):441-448.
Anti-Metastatic Effect of Dehydrocorydaline on H1299 Non-Small Cell Lung Carcinoma Cells via Inhibition of Matrix Metalloproteinases and B Cell Lymphoma 2.
Though Dehydrocorydaline, an alkaloid isolated from Corydalis turtschaninovii tuber, was known to have anti-coronary artery disease, anti-inflammatory, apoptotic, anti-allergic, anti-acetylcholinesterase, and antitumor effects, the underlying anti-metastatic mechanism of Dehydrocorydalin was never elucidated in lung cancer cells so far.
METHODS AND RESULTS:
Thus, in the present study, the anti-metastatic effect of Dehydrocorydaline was examined in non-small cell lung carcinoma (NSCLC) cells, mainly targeting matrix metalloproteinases (MMPs) and B cell lymphoma-2 (Bcl-2) signaling. Here, Dehydrocorydaline exerted weak cytotoxicity and attenuated the protein expression of Bcl-2 and activated Bax in a concentration-dependent manner in NSCLC cells, such as A549, H460, H1299, and H596 cells. Also, Dehydrocorydaline suppressed the migration of H1299 cells by wound healing assay and transwell migration assay. Consistently, Dehydrocorydaline attenuated mRNA and protein levels of MMP7 and MMP9 as metastasis biomarkers in H1299 cells by quantitative reverse transcription polymerase chain reaction. Of note, Bcl-2 overexpression reduced the cytotoxic and anti-metastatic effects of Dehydrocorydaline on pCDNA-Bcl-2 transfected H1299 cells.
CONCLUSIONS:
Overall, our findings provide scientific evidence that Dehydrocorydaline exerts anti-metastatic potential via suppression of MMPs and Bcl-2 signaling in NSCLC cells.
Mol Med Rep. 2016 Oct;14(4):3029-36.
Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activation.
Muscle regeneration is a coordinated process that involves proliferation and differentiation of muscle progenitor cells. Activation of MyoD is a key event in myogenic differentiation, which is regulated by p38 mitogen‑activated protein kinases (MAPK). In a screen of natural compounds for the enhancement of MyoD activity, Dehydrocorydaline (DHC) from the Corydalis tuber was identified.
METHODS AND RESULTS:
Treatment of C2C12 myoblasts with DHC increased the expression levels of muscle‑specific proteins, including MyoD, myogenin and myosin heavy chain. In addition, C2C12 myoblasts exhibited enhanced multinucleated myotube formation without any cytotoxicity. Treatment with DHC elevated p38 MAPK activation and the interaction of MyoD with an E protein, which is likely to result in activation of MyoD and promotion of myoblast differentiation. Furthermore, defects in differentiation‑induced p38 MAPK activation and myoblast differentiation induced by depletion of the promyogenic receptor protein Cdo in C2C12 myoblasts were restored by DHC treatment.
CONCLUSIONS:
In conclusion, these results indicated that DHC stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. These findings suggested that DHC may be considered a potential therapeutic compound for the improvement of muscle stem cell regenerative capacity in injured muscle.
Sci Rep. 2016 Jun 7;6:27129.
Antinociceptive effects of dehydrocorydaline in mouse models of inflammatory pain involve the opioid receptor and inflammatory cytokines.
Dehydrocorydaline (DHC) is an alkaloidal component isolated from Rhizoma corydalis. Previous studies have shown that DHC has anti-inflammatory and anti-tumor effects and that it can protect the cardiovascular system. However, there are few studies of the antinociceptive effects of DHC in vivo.
METHODS AND RESULTS:
This study explored the antinociceptive effects and possible mechanisms of DHC in mice using two inflammatory pain models: the acetic acid-induced writhing test and the formalin paw test. The intraperitoneal administration of DHC (3.6, 6 or 10 mg/kg) showed a dose-dependent antinociceptive effect in the acetic acid-induced writhing test and significantly attenuated the formalin-induced pain responses in mice. The antinociceptive effects of DHC were not associated with changes in the locomotor activity or motor responses of animals, and no obvious acute or chronic toxic effects were observed in the mice. Furthermore, the use of naloxone confirmed the involvement of the opioid receptor in the central antinociceptive effects of DHC. DHC reduced formalin-induced paw edema, which indicated that DHC may produce an anti-inflammatory effect in the periphery. In the formalin test, DHC decreased the expression of caspase 6 (CASP6), TNF-α, IL-1β and IL-6 proteins in the spinal cord.
CONCLUSIONS:
These findings confirm that DHC has antinociceptive effects in mice.
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
Dehydrocorydalin (CAS number: 30045-16-0) is an important natural alkaloid mainly found in the genus Corydalis of the Ranunculaceae family. As one of the common active ingredients in traditional Chinese medicine, dehydroquercetin has received widespread attention in recent years due to its diverse pharmacological activities, especially its potential in the field of analgesia. With the development of modern pharmacology and molecular biology techniques, the pharmacological mechanism and target of dehydroquercetin have gradually been revealed, providing a theoretical basis for its clinical application.
This review aims to systematically summarize the chemical structure and physicochemical properties, plant sources, and extraction methods of dehydroquercetin, elaborate on its pharmacological activity and mechanism of action, evaluate its pharmacological properties and pharmacokinetic characteristics, explore its clinical application prospects and future research directions, and provide reference for research in the field of natural product pharmacology.
Dehydrocysteine is an isoquinoline alkaloid with the molecular formula C21H23NO5 and a molecular weight of 366.43. Its structural features include a nitrogen-containing isoquinoline skeleton, multiple methoxy substituents, and ester groups, endowing it with high chemical stability and specific biological activity. The topological polar surface area (TPSA) of dehydrogenated purple violet alkaloid is 55.84 Å ², with 5 hydrogen bond acceptors, indicating its moderate polarity and favorable binding with biomolecules.
In terms of physical and chemical properties, dehydroquercetin has a low solubility in water, but it dissolves well in organic solvents such as methanol and ethanol. Its blood-brain barrier penetration ability has been assessed as low, suggesting that its direct effects in the central nervous system may be limited, but this may also reduce the risk of central side effects. There is currently insufficient data reporting on safety indicators such as hepatotoxicity, cardiotoxicity, and hERG channel inhibition, and further experimental verification is needed.
The main source of dehydroquercetin is the genus Corydalis in the Ranunculaceae family, especially medicinal plants such as Corydalis yanhusuo (Corydalis yanhusuo). As a traditional Chinese medicine, Corydalis yanhusuo has always been used for promoting blood circulation, removing blood stasis, and relieving pain. Its active ingredient is rich in dehydroquercetin.
The extraction process usually adopts organic solvent extraction method, combined with acid-base adjustment and liquid-liquid distribution technology, to improve the extraction efficiency and purity of dehydroquercetin. The specific steps include:
Modern separation techniques such as high-performance liquid chromatography (HPLC) and supercritical fluid extraction (SFE) have also been applied to the extraction and purification of dehydroquercetin, improving yield and purity.
The pharmacological activities of dehydroquercetin are mainly reflected in analgesic, anti-inflammatory, antidepressant, and neuroprotective aspects, with the most in-depth research on analgesic effects.
Multiple in vitro and in vivo experiments have shown that dehydroquercetin has significant analgesic effects. Its analgesic effect showed good dose-dependent effects in hot plate experiments, acetic acid-induced writhing tests, and inflammatory pain models. Compared with traditional opioid analgesics, dehydroquercetin exhibits lower addiction and resistance risks.
Dihydroquercetin can inhibit the release of various inflammatory mediators, such as prostaglandins (PGE2) and cyclooxygenases (COX-1, COX-2), and alleviate inflammatory responses. Its anti-inflammatory effect has been validated in experimental arthritis and inflammation models.
Dihydroquercetin exhibits certain neuroprotective and antidepressant potential by regulating the neurotransmitter system, particularly the dopamine and 5-hydroxytryptamine systems. Related studies have shown that it can improve functional recovery after nerve injury and alleviate depressive like behavior.
The mechanism of action of dehydroquercetin involves multiple molecular targets, especially in the field of analgesia, exhibiting the characteristic of multi-target synergistic regulation.
TRPV1 and TRPA1 are ion channels in sensory nerve endings that participate in the transmission and perception of pain signals. Dihydroquercetin exerts analgesic effects by regulating the activity of these two channels, inhibiting the transmission of pain signals.
Dihydroquercetin can bind to three types of opioid receptors, μ, δ, and κ, activate the opioid system, and produce analgesic effects. Compared with traditional opioid drugs, its excitatory activity is weaker, which may reduce the common side effects of opioid drugs.
CNR1 receptors regulate pain and emotion in the central nervous system. Dehydrocorydrine participates in pain relief and emotion regulation by regulating the activity of CNR1 receptors.
Dihydroquercetin inhibits the activity of COX-1 and COX-2 enzymes, reduces prostaglandin synthesis, lowers inflammatory response and pain perception.
By regulating the serotonin transporter (SERT) and dopamine D2 receptor, dehydroquercetin affects the balance of neurotransmitters and exerts antidepressant and neuroprotective effects.
In summary, dehydroquercetin regulates pain and related pathological states through multi-target and multi pathway synergistic effects, reflecting its complex pharmacological network characteristics.
The pharmacological parameters of dehydroquercetin show that it has certain development potential, but there are also challenges.
The molecular weight is 366.43, TPSA is 55.84, and the number of hydrogen bond acceptors is 5, which meets most of the requirements of Lipinski's rule, indicating that it has good oral bioavailability potential. The blood-brain barrier has a low penetration ability, which may limit the direct action of the central nervous system, but helps to reduce central toxicity.
At present, there is a lack of data on the hepatotoxicity, cardiotoxicity (including hERG channel inhibition), and genotoxicity (Ames test) of dehydroquercetin, and systematic toxicological studies are needed to clarify its safety.
There are few existing literature reports, and preliminary studies have shown that dehydroquercetin is widely distributed in the body, but the metabolic pathways and clearance mechanisms are not yet clear. In the future, systematic pharmacokinetic studies need to be conducted, including absorption, distribution, metabolism, and excretion (ADME) characteristics, to guide clinical dosage form design and dosing regimen optimization.
As a natural alkaloid, dehydroquercetin has broad application prospects in the fields of chronic pain, inflammatory diseases, and neurological and psychiatric disorders due to its multi-target analgesic mechanism and potential anti-inflammatory and neuroprotective effects.
Given its regulatory effects on multiple targets such as TRPV1 and opioid receptors, dehydroquercetin is expected to become a candidate molecule for novel analgesic drugs, particularly suitable as an alternative therapy for patients with opioid tolerance or dependence.
The anti-inflammatory and neuroprotective effects of dehydroquercetin provide the possibility for its application in inflammatory and neurodegenerative diseases. In the future, it can be combined with modern drug delivery technology to enhance its bioavailability and targeting.
Despite exhibiting good pharmacological activity, the pharmacological properties, safety, and pharmacokinetic characteristics of dehydroquercetin still require further research. Future work should focus on:
In addition, combining modern molecular docking and drug design techniques to deeply analyze its molecular target mechanism of action will help promote the drug development process of dehydroquercetin.
Dihydroquercetin, as a natural alkaloid with multi-target effects, exhibits significant analgesic and anti-inflammatory activities and has good potential for drug development. Its complex mechanism of action provides new ideas for the development of novel analgesic and neuroprotective drugs. In the future, through systematic pharmacological, toxicological, and pharmacokinetic studies, combined with modern drug design and clinical validation, it is expected to promote the clinical application of dehydroquercetin and benefit patients. The continuous development of pharmacology of natural products will provide a solid scientific foundation for the development of drugs such as dehydroquercetin and similar natural compounds.
