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℃

Introduction/Overview

Dehydrocorydalin (CAS No.: 30045-16-0) is an important natural alkaloid mainly found in the genus Corydalis (Corydalis spp.) of the Ranunculaceae family. As one of the common active ingredients in traditional Chinese medicine, dehydrovioline has attracted widespread attention in recent years due to its diverse pharmacological activities, especially its potential in pain relief. With the development of modern pharmacology and molecular biology techniques, the pharmacological mechanisms and targets of dehydrocytinine have gradually been revealed, providing a theoretical foundation for its clinical application.

This review aims to systematically summarize the chemical structure and physicochemical properties of dehydropurulinine, plant origin, and extraction methods, elaborate in detail on its pharmacological activity and mechanism of action, evaluate its druggability and pharmacokinetic characteristics, explore its clinical application prospects and future research directions, and provide a reference for research in the field of natural product pharmacology.

Chemical structure and physicochemical properties

Dehydropurine alkaloid 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, which give it high chemical stability and specific biological activity. The topological surface area (TPSA) of dehydroviolet alkaloid is 55.84 Ų, and the number of hydrogen bond acceptors is 5, indicating moderate polarity that facilitates binding with biomacromolecules.

In terms of physical and chemical properties, dehydrovioline soda has low solubility in water but dissolves well in organic solvents such as methanol and ethanol. Its blood-brain barrier penetration ability was assessed as low, suggesting that its direct effect in the central nervous system may be limited, but this may also reduce the risk of central side effects. There is currently no sufficient data on safety indicators such as hepatotoxicity, cardiotoxicity, and hERG channel inhibition, and further experimental validation is needed.

Plant Origins and Extraction Methods

Dehydropurine mainly comes from Ranunculaceae plants in the genus Corydalis, especially medicinal plants such as Corydalis yanhusuo. As a traditional Chinese medicine, Corydalis has traditionally been used to promote blood circulation, remove blood stasis, relieve pain, and relieve pain. Its active ingredient is rich in dehydrovioline alkaloids.

The extraction process typically uses organic solvent extraction methods, combined with acid-base adjustment and liquid-liquid distribution techniques to improve the extraction efficiency and purity of dehydropurine alkaloid. The specific steps include:

1. After drying and crushing, the raw materials are extracted by reflux using ethanol or methanol as solvents.
2. After concentration, the extract is adjusted to alkalinity and separated using organic solvents (such as chloroform or ethyl acetate).
3. Further purification by column chromatography (silica gel or C18 reversed-phase column) yields high-purity dehydropurine alkaloids.

Modern separation technologies such as high-performance liquid chromatography (HPLC) and supercritical fluid extraction (SFE) are also applied to the extraction and purification of dehydropurine alkaloids, improving yield and purity.

Pharmacological activity research

The pharmacological activity of dehydrocytinine mainly manifests in analgesia, anti-inflammation, antidepressant, and neuroprotection, with its analgesic effects being the most extensively studied.

Analgesic effect

Multiple in vivo and in vitro experiments have shown that dehydrovioline has significant analgesic effects. Its analgesic effect demonstrated good dose-dependency in hot plate experiments, acetic acid-induced torsion tests, and inflammatory pain models. Compared to traditional opioid analgesics, dehydrovioline shows a lower risk of addiction and resistance.

Anti-inflammatory effects

Dehydropurine can inhibit the release of various inflammatory mediators, such as prostaglandins (PGE2) and cyclooxygenases (COX-1, COX-2), reducing inflammatory responses. Its anti-inflammatory effects have been validated in experimental arthritis and inflammation models.

Neuroprotective and antidepressant effects

Dehydrovioline demonstrates certain neuroprotective and antidepressant potential by regulating the neurotransmitter system, especially dopamine and serotonin. Related studies have shown that it can improve functional recovery after nerve injury and reduce depressive-like behaviors.

Mechanism of action and molecular targets

The mechanism of action of dehydrovioline involves multiple molecular targets, especially in the field of analgesia, showing multi-target coordinated regulation.

TRPV1 and TRPA1 channels

TRPV1 and TRPA1 are ion channels at sensory nerve endings that participate in the transmission and perception of pain signals. Dehydrovioline regulates the activity of these two channels, inhibits pain signal transmission, and exerts its analgesic effect.

Opioid receptors (OPRM1, OPRD1, OPRK1)

Dehydropuruline can bind to three opioid receptors: μ, δ, and κ, activating the opioid system and producing analgesic effects. Compared to traditional opioids, it has weaker agonizing activity and may reduce the common side effects of opioids.

Cannabinoid receptor CNR1

CNR1 receptors regulate pain and emotions in the central nervous system. Dehydrovioline participates in pain relief and mood regulation by modulating CNR1 receptor activity.

Cyclooxygenases (PTGS1, PTGS2)

Dehydrovioline inhibits the activity of COX-1 and COX-2 enzymes, reduces prostaglandin synthesis, and lowers inflammatory responses and pain perception.

The monoamine transporter SLC6A4 and the dopamine receptor DRD2

By regulating the serotonin transporter (SERT) and dopamine D2 receptors, dehydropurine affects neurotransmitter balance, exerting antidepressant and neuroprotective effects.

In summary, dehydrovioline regulates pain and related pathological states through multi-target and multi-pathway synergistic effects, reflecting its complex pharmacological network characteristics.

Druggability evaluation and pharmacokinetics

The druggability parameters of dehydropuruline indicate that it has certain development potential, but there are also challenges.

Drug similarity and physicochemical properties

With a molecular weight of 366.43, TPSA of 55.84, and a hydrogen bond receptor number of 5, it meets most of the requirements of the Lipinski rule, indicating good oral bioavailability potential. The blood-brain barrier has a lower penetration capacity, which may limit direct action by the central nervous system, but it helps reduce central toxicity.

Safety evaluation

Currently, data on hepatotoxicity, cardiotoxicity (including hERG channel inhibition), and genotoxicity (Ames assay) of dehydrovioline are lacking, requiring systematic toxicological studies to determine its safety.

Pharmacokinetic characteristics

There are few existing literature reports, and preliminary studies suggest that dehydrovioline is widely distributed in the body, but its metabolic pathway and clearance mechanisms remain unclear. In the future, systematic pharmacokinetic studies, including absorption, distribution, metabolism, and excretion (ADME) characteristics, are needed to guide clinical formulation design and administration protocol optimization.

Prospects and outlooks for clinical applications

As a natural alkaloid, dehydrovioline has broad application prospects in chronic pain, inflammatory diseases, and neuropsychiatric disorders due to its multi-target analgesic mechanism and potential anti-inflammatory and neuroprotective effects.

Development of analgesic drugs

Given its regulatory effects on multiple targets such as TRPV1 and opioid receptors, dehydropurine alkaloid is expected to become a candidate molecule for novel analgesics, especially suitable for alternative therapy in patients who tolerate opioids or depend on them.

Anti-inflammatory and neuroprotection

The anti-inflammatory and neuroprotective effects of dehydrovioline offer potential applications in inflammatory and neurodegenerative diseases. In the future, combined with modern drug delivery technologies, its bioavailability and targeting potential can be improved.

R&D challenges and future directions

Although dehydrocylindrine exhibits good pharmacological activity, its druggability, safety, and pharmacokinetic characteristics still require further study. Future work should focus on:

• Systematic toxicological assessment to ensure safety.
• Clarification of pharmacokinetics and metabolic mechanisms.
• Structural optimization and derivative design to enhance activity and pharmacokinetic performance.
• Preclinical and clinical studies to verify efficacy and safety.

Moreover, by integrating modern molecular docking and drug design technologies, in-depth analysis of its molecular target mechanisms will help advance the drug development process of dehydropuruline alkaloids.

Conclusion

Dehydropurine alkaloids, as a natural alkaloid with multi-target effects, exhibit significant analgesic and anti-inflammatory activities and have good pharmaceutical potential. Its complex mechanism of action offers new ideas for developing novel analgesic and neuroprotective drugs. In the future, through systematic pharmacology, toxicology, and pharmacokinetic studies, combined with modern drug design and clinical validation, it is expected to promote the translation of dehydropurine alkaloid into clinical applications, benefiting patients. The ongoing development of natural product pharmacology will provide a solid scientific foundation for the development of drugs such as dehydrocytinine and similar natural compounds.