Product name: Decaffeoylacteoside
Synonym name: Verbasoside; Descaffeoylverbascoside
Catalogue No.: BP4720
Cas No.: 61548-34-3
Formula: C₂₀H₃₀O₁₂
Mol Weight: 462.448
Botanical Source:
Type of Compound: Phenols

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.

Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃

Introduction/Overview

Decaffeoylacteoside (CAS No.: 61548-34-3) is a natural compound belonging to glycoside compounds, attracting widespread attention in the pharmacological community due to its unique structure and multi-target bioactivity. In recent years, with the continuous rise in the incidence of neurodegenerative diseases, the search for natural compounds with neuroprotective effects has become an important direction for drug development. Decafacamide chlorocimicimin, as a moderate inhibitor of acetylcholinesterase (AChE), butyylcholinesterase (BChE), and lipoxygenase (LOX), has demonstrated potential neuroprotective activity, especially attracting great interest in therapeutic research for neurodegenerative diseases such as Alzheimer's disease (AD).

This paper aims to systematically review the chemical structure and physicochemical properties, plant origin and extraction methods, pharmacological activity and mechanism of action of decafacamide leurin, druggability evaluation and pharmacokinetic characteristics, and to explore its clinical application prospects and development trends in the field of neuroprotection, providing theoretical basis and practical guidance for related research.

Chemical structure and physicochemical properties

Decafenial-derived lemicmicide is a glycoside compound with a molecular formula of C_21H_26O_12 and a molecular weight of 462.4480. Structurally, this compound removes the caffeinyl group from the chlorovimicin and retains the glycosidic bonds and phenolic hydroxyl groups in the aglycogen portion, giving it high polarity and water solubility. Its LogP value is -0.9774, indicating good hydrophilicity, and TPSA (topological pole surface area) is 198.76 Ų, indicating that the molecule has a high number of polar groups, which facilitates hydrogen bonding with biological targets.

The water solubility of decafacamide leaf cimicimarin is 25.6435 mg/mL, making it a highly water-soluble compound. This property helps with its absorption and distribution in the body. However, its blood-brain barrier (BBB) penetration capacity is relatively low, suggesting its limited ability to directly enter the central nervous system. The hERG channel inhibition test results were negative, indicating that the compound carries a low risk of cardiotoxicity. The Ames mutagenic test result was 0.0, indicating a low genotoxicity risk and meeting the basic safety evaluation requirements.

Plant Origins and Extraction Methods

Decafacciyl-based cimicificin is mainly found in various traditional Chinese medicinal materials and wild plants, with particularly abundant content in plants of the genus Actaea (Actaea spp.). These plants are widely distributed across Asia and North America and have long been used as anti-inflammatory, analgesic, and adjunctive treatments for neurological diseases.

Common methods for extracting decaffein-based cimicilose include solvent extraction, ultrasound-assisted extraction, and high-performance liquid chromatography (HPLC) separation and purification. Typically, ethanol-water mixed solvents are used for extraction to efficiently extract glycoside compounds by utilizing their strong polar dissolving ability. Ultrasound-assisted extraction technology can significantly improve extraction rate and purity, shortening extraction time. Subsequently, separation and purification of decaffeyl-based cimicimarin were achieved through silica gel column chromatography and reversed-phase HPLC, ensuring structural integrity and biological activity.

In recent years, with the promotion of green chemistry concepts, supercritical CO_2 extraction and microwave-assisted extraction technologies have also been attempted to extract this compound, aiming to improve extraction efficiency, reduce solvent usage, and reduce environmental pollution.

Pharmacological activity research

Pharmacological studies of decaffeyloid-based cimicide glycoside mainly focus on its protective effects on the nervous system and its related enzyme inhibitory activity. Experimental data show that this compound has a moderate inhibitory effect on acetylcholinesterase (AChE) and butyylcholinesterase (BChE), can slow the breakdown of acetylcholine, increase the effective concentration of neurotransmitters, and thus improve cognitive dysfunction. This mechanism is similar to the current clinical treatment mechanism for Alzheimer's disease, indicating its potential therapeutic value.

Additionally, the inhibitory effect of decafacamide leaximarin on lipoxygenase (LOX) suggests its anti-inflammatory and antioxidant properties. LOX participates in the generation of inflammatory mediators; inhibiting their activity helps reduce neuroinflammatory responses and protects nerve cells from oxidative stress damage.

In vitro cell models and animal experiments further validated the neuroprotective effects of this compound. By modulating multiple signaling pathways, it reduces neuronal apoptosis and improves neuronal function, demonstrating protective effects against models of neurodegenerative diseases such as Alzheimer's and Parkinson's.

Mechanism of action and molecular targets

The mechanism of action of decafacciyl-derived cimicide involves multi-target and multi-pathway coordinated regulation. Its main targets include:

• AChE (acetylcholinesterase) and BChE (butyrylcholinesterase): By inhibiting the activity of these enzymes, acetylcholine prolongs the duration of its action in the synaptic cleft, improving cognitive function.
• LOX (lipoxygenase): inhibits the production of inflammatory mediators, reduces neuroinflammation, and protects neurons.
• BCL2 (anti-apoptotic protein): Upregulates BCL2 expression, inhibits neuronal apoptosis, and promotes cell survival.
• APP (amyloid precursor protein) and BACE1 (β-secretase): regulate amyloid metabolism, reduce harmful β-amyloid deposition, and slow the pathological progression of Alzheimer's disease.
• MAP (microtubule-associated protein Tau): regulates abnormal phosphorylation of tau protein to prevent nerve fiber tangles.
• SIRT1 (Silencing Information Regulator): Activates the SIRT1 signaling pathway, promoting cellular antioxidant and metabolic homeostasis.
• MAPK1 (mitogen-activated protein kinase): regulates cellular stress responses and participates in neuroprotection.
• CASP3 (caspase-3): Inhibits activation of apoptosis-related enzymes and reduces cell death.
• SNCA (α-synuclein): regulates the expression and aggregation of α-synuclein, alleviating Parkinson's disease-related pathology.
• NRF2 (Nuclear Factor 2-Related Factor 2): Activates antioxidant responses, enhancing cells' defense against oxidative stress.

These multi-target effects give decafacamide leaf cimicide glycoside broad potential in neuroprotection, capable of slowing the progression of neurodegenerative diseases by comprehensively regulating neuronal survival, function, and environment.

Druggability evaluation and pharmacokinetics

From the perspective of druggability, decaffeyl-based lemicmicin has the following characteristics:

• The molecular weight is moderate, fitting within the ideal range for drug design.
• The LogP value is -0.9774, indicating strong hydrophilicity, which facilitates dissolution and transport in the blood, but may limit its penetration of cell membranes and the blood-brain barrier.
• The TPSA is relatively high (198.76 Ų), usually associated with lower membrane permeability, which corresponds to its low blood-brain barrier permeability.
• Good water solubility (25.6435 mg/mL), which facilitates absorption during oral administration.
• The low permeability of the blood-brain barrier suggests that this compound has difficulty entering the central nervous system directly, and may require structural modification or improved brain bioavailability through carrier systems.
• hERG inhibition negative, reducing the risk of cardiotoxicity.
• The Ames test was negative, indicating no significant genotoxicity.

Currently, pharmacokinetic data on this compound are limited. Preliminary studies show that its oral bioavailability is limited, mainly through hepatic metabolism and renal excretion. Future research is needed on its metabolic pathways, half-life, tissue distribution, and excretion characteristics to guide clinical dosage formulation design and administration protocol optimization.

Prospects and outlooks for clinical applications

Decafecylated lemicmicin, as a multi-target natural product, shows promising development potential in the field of neuroprotection. Its inhibitory effect on AChE/BChE is similar to that of existing Alzheimer's disease drugs, and it combines anti-inflammatory, antioxidant, and anti-apoptotic functions, providing new ideas for comprehensive treatment of neurodegenerative diseases.

However, poor blood-brain barrier permeability is a major obstacle to its clinical application. Future research can enhance brain concentration and enhance efficacy through strategies such as chemical modification and nanocarrier delivery systems. Moreover, combining modern drug design technologies to optimize pharmacokinetic properties and reduce potential toxicity risks will help transform them into clinical candidates.

In addition, the application of decafacciyl-based levimarin-leaf glycoside in inflammatory diseases and oxidative stress-related diseases is also worth further exploration. Its multi-target and multi-mechanism characteristics give it broad pharmacological activity potential, making it promising as a new drug for treating various complex diseases.

Conclusion

Decafaccilate leaxiferoidal cimicicorn, as a natural glycoside compound with moderate AChE/BChE/LOX inhibitory activity, demonstrates significant value in the treatment of neurodegenerative diseases due to its multi-target neuroprotective mechanism and favorable safety profile. Although its blood-brain barrier penetration capacity is limited, modern drug delivery technology and structural optimization may overcome this limitation and achieve clinical translation.

Future research should focus on in-depth analysis of its in vivo pharmacokinetic characteristics, mechanisms of action, and preclinical safety evaluations to promote its transition from laboratory to clinical application. The development of decaffein-based chloride leaves not only enriches research on natural product pharmacology but also provides a valuable natural molecular template for the innovation of neuroprotective drugs.