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Product name: Evolitrine
Synonym name:
Catalogue No.: BP4230
Cas No.: 523-66-0
Formula: C13H11NO3
Mol Weight: 229.235
Botanical Source: Euodiae fructus
Type of Compound: Alkaloids
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.
The product could be supplied from milligrams to grams
Inquire for bulk scale.
For Reference Standard and R&D, Not for Human Use Directly.
HPLC of Evolitrine
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
44.4900
2.5022
2.5015
.0237
3.2134
31.5565
High
86.8659
2.3663
Yes
No
Yes
No
Yes
Yes
1.8
No
No
Yes
No
Natural products, as an important source of drug discovery, hold an irreplaceable position in modern medical research. Evolitrine (CAS No.: 523-66-0) is a natural alkaloid isolated from the plant Acronychia pedunculata, widely recognized for its remarkable anti-inflammatory activity. As the pathological basis of various diseases, inflammatory responses have complex and diverse regulatory mechanisms, involving various cytokines, signaling pathways, and enzymes. Evodia Cornus Folline demonstrates strong anti-inflammatory potential by modulating multiple key inflammation-related targets, making it a strong candidate for natural anti-inflammatory drug development. This paper systematically reviews the chemical structure and physicochemical properties of evodia inflorescine (evodia inflorescence), plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and pharmacokinetic characteristics, aiming to provide scientific basis and theoretical support for its clinical application and subsequent research.
Evolitrine (7-Methoxydictamnine, Evolitrine) has the molecular formula C13H15NO3 and a molecular weight of 229.2350. Its structural feature is an alkaloid framework containing methoxy-substituted alkaloid groups, featuring typical indole alkaloid structural units. The LogP value of evodia caline is 2.5022, indicating moderate lipid solubility, which facilitates cell membrane penetration and distribution in vivo. The polar surface area (TPSA) is 44.49 Ų, indicating moderate molecular polarity, which is conducive to binding to biological targets. Low water solubility (0.0237 mg/mL) suggests limited solubility in the aqueous phase, which may affect oral bioavailability. The blood-brain barrier has high permeability, indicating its potential for central nervous system function. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test result was 1.8, indicating a low genotoxicity risk and meeting the basic requirements for safe medication.
Evodia root was originally isolated from Acronychia pedunculata, a plant in the Rutaceae family. This plant is widely distributed in tropical and subtropical regions and has traditionally been used to treat various inflammation-related diseases. During extraction, organic solvents (such as ethanol and methanol) are typically used to extract dried plant material, followed by separation and purification techniques such as liquid-liquid partitioning and column chromatography to obtain evodia spring alkalin. High-performance liquid chromatography (HPLC) and mass spectrometry (MS) technologies are widely used for qualitative and quantitative analysis. In recent years, new extraction technologies such as ultrasound-assisted extraction and microwave-assisted extraction have also been attempted to extract evodia spring alkaloid to improve yield and purity.
The main pharmacological activity of evodia is concentrated in its anti-inflammatory effect. Both in vitro cell models and in vivo animal inflammation models have confirmed that it significantly inhibits the release of inflammatory mediators and activates inflammatory cells. Specifically, it inhibits the expression of pro-inflammatory factors such as IL-6 and TNF-α, and reduces the activity of inflammation-related enzymes like PTGS1 (COX-1), PTGS2 (COX-2), and NOS2 (iNOS). Evodia Cornus vernal also exhibits regulatory effects on the inflammation-related ion channels TRPV1 and TRPA1, reducing pain and neuroinflammatory responses. Its anti-inflammatory effects have been demonstrated in various models of inflammatory diseases, including arthritis, inflammatory bowel disease, and neuroinflammation.
Additionally, the regulation of apoptosis-related protein CASP1 by evodia indicates suggests its potential role in programmed death of inflammation-related cells. Its inhibition of key transcription factor NFKB1 and signal transduction protein STAT3 further reveals the molecular mechanisms underlying its anti-inflammatory mechanism.
The anti-inflammatory mechanism of evodia intrinsic aline involves multiple signaling pathways and various molecular targets. First, it reduces the amplification of inflammatory signals by inhibiting the expression of pro-inflammatory cytokines IL-6 and TNF-α. IL-6, as an important mediator of inflammatory responses, can activate the STAT3 signaling pathway and promote transcription of inflammatory genes. Evodia invertine inhibits STAT3 phosphorylation and activation, blocking the transmission of inflammatory signals.
Second, evodia incubine regulates NFKB1 activity, inhibits its nuclear translocation, and reduces the expression of inflammation-related genes. The NFKB signaling pathway is the core regulatory pathway of inflammatory responses, and its overactivation is closely linked to various chronic inflammatory diseases. Evodia inertine exerts anti-inflammatory and tissue-protective effects by inhibiting this pathway.
Additionally, evodia inhibits the inflammation-related enzymes PTGS1 and PTGS2, reduces prostaglandin synthesis, and alleviates inflammatory symptoms. Inhibition of NOS2 reduces the production of excess nitric oxide, alleviating oxidative stress and inflammatory damage.
In the field of neuroinflammation, evodia inertine modulates TRPV1 and TRPA1 ion channels, reducing inflammatory pain and nerve sensitivity. CASP1, as a key enzyme for activating inflammasomes, participates in the maturation and release of pro-inflammatory cytokines. Inhibition by evodia invertine further blocks the inflammatory cascade.
Overall, evodia inertine regulates the inflammatory microenvironment through multi-target and multi-pathway synergistic effects, demonstrating promising anti-inflammatory potential.
The druggability parameters of evodia inertine indicate that it has promising potential for drug development. The molecular weight of 229.2350 complies with the Lipinski rule, with a moderate LogP value of 2.5, which benefits drug membrane permeability and oral absorption. The TPSA value of 44.49 Ų is lower than 140 Ų, indicating good cell membrane penetration capability. Lower water solubility may limit its oral bioavailability, but drug formulation technologies such as nanocarriers and solid dispersions can improve solubility.
The high permeability of the blood-brain barrier indicates the potential of evodia intrinsic aline for the treatment of central nervous system-related inflammatory diseases. Negative hERG suppression suggests a lower risk of cardiotoxicity and better safety. Ames test results showed that the genotoxicity risk is low and meets safe medication standards.
Currently, pharmacokinetic research on evodia inertine is relatively limited. Preliminary in vivo experiments show that it is rapidly absorbed and widely distributed, with metabolic pathways possibly involving the liver's CYP450 enzyme system, and excretion mainly via the kidneys. Future studies are needed to systematically study its absorption, distribution, metabolism, and excretion (ADME) characteristics to guide clinical dosage form design and drug regimen optimization.
Given the remarkable anti-inflammatory activity and good druggability of evodia inertine, it has broad application prospects in the treatment of inflammatory diseases. Especially in rheumatoid arthritis, inflammatory bowel disease, neuroinflammation, and chronic pain management, evodia cornelian uproline is expected to become a new natural anti-inflammatory drug.
Future research should focus on the following aspects: first, to deeply analyze its molecular mechanisms, especially its interaction with inflammatory signaling pathways and regulatory networks; Second, conduct systematic pharmacokinetic and toxicological studies to ensure safety and efficacy; Third, explore multiple delivery routes and dosage forms to enhance bioavailability and targeting; Fourth, conduct preclinical animal models and clinical trials to verify their therapeutic effects and safety.
In addition, the potential of evodia inertine in combination with other anti-inflammatory drugs, as well as its applications in immunomodulatory and anti-tumor fields, are also worth further exploration. By integrating modern drug design and synthetic biology techniques, optimizing its structure and pharmacodynamic properties will further promote the clinical translation of evodia inflorescine.
As a natural alkaloid derived from Acronychia pedunculata, evodia has shown great potential as a new anti-inflammatory drug due to its multi-target anti-inflammatory effects and excellent druggability. By regulating key inflammatory targets such as IL-6, STAT3, NFKB1, PTGS1/2, NOS2, and TRPV1/TRPA1, it effectively suppresses inflammatory responses and reduces tissue damage. Although pharmacokinetics and clinical application research are still in the early stages, their safety and bioactivity provide a solid foundation for subsequent development. In the future, both basic and applied research should be strengthened to promote the clinical translation of evodia intrinsic capillarine, providing new treatment options for patients with inflammatory diseases.
Shenshuai
Wenjing
Hedandan
