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Product name: Atranorin
Synonym name: Atranorine;Parmelin; Parmelin Acid; Usnarin; Usnarin Acid
Catalogue No.: SBP60027
Cas No.: 479-20-9
Formula: C19H18O8
Mol Weight: 374.345
Botanical Source:
Physical Description:
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
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 Atranorin
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
130.3600
3.2557
1.7229
.2145
5.0206
3.0228
Low
88.9851
2.8195
Yes
No
Yes
No
No
Yes
0.6
No
No
Yes
No
Atranorin (CAS No.: 479-20-9) is a typical secondary lichen metabolite, belonging to the benzoic acid phenolic compound with abundant biological activity. In recent years, lychetin has become a research hotspot in the field of natural product pharmacology due to its multi-target and multifunctional pharmacological properties. Its remarkable antibacterial, anti-inflammatory, antioxidant, anti-glycation, analgesic, and antitumor activities give it potential application value in various disease models, especially showing promising prospects in the treatment of myelodysplastic syndromes, tumors, and inflammation-related diseases.
As an inhibitor of the Akt signaling pathway, lychitinin can regulate cell proliferation, apoptosis, and metabolic processes, revealing its potential mechanisms in tumor treatment. In addition, its ability to scavenge free radicals (DPPH and ABTS radical scavenging IC50 are 117 μM and <10 μM respectively) and promote wound healing, further expanding its pharmacological application range. This paper will systematically review the chemical structure and physicochemical properties of lychetin, plant origin and extraction methods, pharmacological activity, mechanism of action, druggability evaluation, and clinical application prospects, aiming to provide theoretical support and research directions for its subsequent drug development and clinical translation.
The chemical name of lychitinin is 3-formyl-7-hydroxy-8-methyl-6-methoxycarbonyl-1,4-dihydroxy-2-naphthoic acid methyl ester, with the molecular formula C19H18O8 and a molecular weight of 374.3450. Its structural core is a benzoquinone backbone derived from benzoic acid, containing multiple hydroxyl and carboxyl functional groups, giving it strong polarity and biological activity. The LogP value of lychetin was 3.2557, indicating moderate lipid solubility, which is beneficial for cell membrane penetration and bioavailability. Its topological pole surface area (TPSA) is 130.36 Ų, reflecting its high polarity and hydrogen bond donor/acceptor capacity, which significantly affects its binding to biomacromolecules.
In terms of water solubility, lychitinin has a water solubility of 0.2145 mg/mL, making it a low-solubility compound, which may limit its oral absorption and bioavailability. The low permeability of the blood-brain barrier suggests limited function in the central nervous system, but also reduces the risk of central toxicity. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity in lychetin, while the Ames mutagenic test result was 0.6, indicating low genotoxicity risk and a solid safety foundation.
Lychetin mainly comes from lichen species, especially various genera such as Cladonia, Stereocaulon, and other lichen family species. As a symbiote, lichens produce large amounts of secondary metabolites to adapt to extreme environments, with lychetin being an important benzoic acid secondary metabolite.
Traditional extraction methods mostly use organic solvent extraction methods, such as ethanol, methanol, or ethyl acetate, combined with ultrasound-assisted extraction or Soxhlet extraction to improve extraction efficiency. The extract undergoes purification steps such as concentration, separation, and column chromatography (silica gel column, reversed-phase C18 column), ultimately obtaining high-purity lychetin. In recent years, green and efficient methods such as supercritical CO2 extraction and microwave-assisted extraction technology have gradually been applied to lychitin extraction, significantly improving extraction efficiency and purity, reducing the use of organic solvents, and aligning with the environmental trend of modern natural product extraction.
Lychetin exhibits inhibitory effects on various Gram-positive and Gram-negative bacteria, especially showing strong antibacterial effects against commonly clinically pathogenic bacteria such as Staphylococcus aureus and Streptococcus pneumoniae. Its antibacterial mechanism may involve multiple pathways including cell membrane destruction, protein synthesis inhibition, and DNA damage, and it also shows certain activity against drug-resistant strains, suggesting its potential as a novel antimicrobial agent.
Lychetin exhibits significant anti-inflammatory activity by inhibiting the release of inflammatory mediators and activating inflammatory signaling pathways. In vivo and in vitro experiments showed that lychetin can downregulate the NF-κB and MAPK signaling pathways, reduce the expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and alleviate inflammatory responses. Additionally, it protects against inflammatory cell infiltration and tissue damage, making it suitable as an adjunct treatment for inflammatory diseases.
Lychitin has significant scavenging ability against DPPH and ABTS free radicals, with IC50s of 117 μM and less than 10 μM, respectively, demonstrating strong antioxidant activity. Its antioxidant mechanism mainly works by activating the Nrf2 signaling pathway, inducing the expression of downstream antioxidant enzymes (such as SOD1, CAT, GPX1, HMOX1, etc.), thereby enhancing cellular antioxidant defense capabilities. Additionally, lychetin can inhibit protein glycation reactions, slow down the formation of AGEs (advanced glycation end products), and has potential anti-diabetic complications.
Lychetin has demonstrated good analgesic effects in various animal models, possibly related to its inhibition of inflammatory mediator release and regulation of neurotransmitters. Its analgesic mechanisms require further research, but evidence already shows it works by regulating central and peripheral pain transmission pathways.
As an Akt inhibitor, lychitinin can block the PI3K/Akt/mTOR signaling pathway, induce tumor cell apoptosis, and inhibit cell proliferation and migration. Multiple in vitro cell experiments and in vivo tumor model studies have shown that lychetin has inhibitory effects on various tumor types, such as breast cancer, lung cancer, colorectal cancer, etc. Its anti-tumor mechanisms involve cell cycle blockade, induction of mitochondria-dependent apoptosis, and inhibition of tumor angiogenesis, demonstrating promising drug development potential.
Lychitin's effect in promoting wound healing mainly works by regulating inflammatory responses, promoting fibroblast proliferation, and collagen synthesis. Experimental results show that lychetin can promote wound closure speed, improve wound tissue structure, and has potential value for wound repair applications.
The multiple pharmacological effects of lychitinin are attributed to its regulation of various molecular targets, with particularly outstanding performance in antioxidant and antitumor fields.
Lychetin enhances cellular antioxidant capacity by activating nuclear factor E2-related factor 2 (Nrf2) and its downstream target genes (such as SOD1, SOD2, CAT, GPX1, HMOX1). As the main regulator of intracellular antioxidant responses, Nrf2's activation promotes the expression of antioxidant enzymes, scavenges excess free radicals, and alleviates oxidative stress damage. In addition, lychetin regulates matrix metalloproteinases (MMP1, MMP3) and tyrosinase (TYR) activities, participating in extracellular matrix remodeling and melanin metabolism, indirectly affecting redox balance.
Lychitinin regulates cell proliferation, apoptosis, and metabolism by inhibiting Akt kinase activity and blocking the PI3K/Akt signaling pathway. The Akt pathway is abnormally activated in various tumor cells, promoting cell survival and drug resistance. The inhibitory effect of lychitinin effectively induces tumor cell apoptosis and suppresses metastasis. Additionally, lychetin may reduce the tumor-promoting effects of the inflammatory microenvironment by modulating signaling pathways such as NF-κB and MAPK.
Lychitin inhibits the expression of pro-inflammatory factors TNF-α, IL-6, and IL-1β, reducing inflammatory responses. Its mechanism involves inhibiting activation of the NF-κB signaling pathway, blocking inflammatory signal transduction, and reducing infiltration of inflammatory cells. Lychitin may also regulate immune cell function and promote the maintenance of immune homeostasis.
The molecular weight of lychitinin (374.3450) and LogP (3.2557) meet the basic requirements of the Lipinski rule, indicating good drug similarity. A higher TPSA (130.36 Ų) suggests strong polarity, which may affect oral absorption and cell membrane penetration. Low water solubility (0.2145 mg/mL) is a major limitation for druggability, and bioavailability needs to be improved through pharmaceutical formulation technology.
The blood-brain barrier has low permeability, making it suitable for treating peripheral diseases and reducing the risk of central nervous system side effects. The hERG channel was inhibited negatively and the Ames test results were good, indicating high safety and low genotoxicity risk.
Currently, pharmacokinetic research on lychetin is relatively limited. Preliminary in vivo experiments show that its oral bioavailability is limited, mainly metabolized by the liver, with a moderate half-life. In the future, further systematic research is needed on its absorption, distribution, metabolism, and excretion (ADME) characteristics to optimize administration regimens and dosage form design.
With its broad pharmacological activity, especially its potential in anti-tumor, anti-inflammatory, and antioxidant fields, lychitinin has promising prospects for clinical translation. As an Akt inhibitor, it is suitable for adjunctive treatment of malignant hematologic diseases such as myelodysplastic syndromes and solid tumors. Moreover, lychitinin's anti-inflammatory and wound healing effects provide new therapeutic approaches for chronic inflammatory diseases and wound repair.
However, the clinical application of lychitinin still faces many challenges, including insufficient bioavailability due to low water solubility, unclear pharmacokinetic characteristics, and a lack of systematic clinical safety evaluation. Future research should focus on optimizing lychetin's formulations, elucidating its in vivo metabolic mechanisms, and preclinical toxicology studies to advance it toward the clinical trial stage.
Additionally, the design and synthesis of lychidin structure-based derivatives, combined with modern medicinal chemistry and computer-aided drug design technologies, are expected to develop candidate drugs with stronger activity and lower side effects. In-depth analysis of the mechanisms of action by multiple targets will also promote the expansion of lychetin's application in the treatment of various complex diseases.
Lychetin, a natural secondary benzoic acid metabolite derived from lichens, has become an important subject of natural product pharmacological research due to its diverse bioactivity and good safety. Its significant effects in antibacterial, anti-inflammatory, antioxidant, anti-glycation, analgesic, and antitumor effects reveal its potential as a multifunctional drug candidate. Although there are still certain limitations in pharmacokinetics and clinical applications, with continuous advances in extraction and purification technologies, drug formulations, and mechanistic research, lychetinin is expected to become an important component of new natural medicines in the future.
Future research should focus on refining the mechanism of action of lychitin, optimizing pharmacokinetics, and evaluating preclinical safety, combined with modern drug development strategies to promote its translation into clinical applications and benefit more patients. Research on lychetin not only enriches the theoretical framework of natural product pharmacology, but also provides new drug resources and therapeutic approaches for the treatment of various diseases.
Shenshuai
Wenjing
Hedandan
