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Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
130.6100
-2.6171
-2.6171
216.0623
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Low
6.2929
4.4927
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0.0
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With the continued rise in global obesity rates, obesity and related metabolic diseases have become significant challenges in the public health sector. Obesity not only increases the risk of cardiovascular disease, type 2 diabetes, fatty liver, and other chronic diseases, but also seriously affects patients' quality of life and lifespan. Currently, drug treatments for obesity are limited and often accompanied by side effects, making the development of safe and effective natural anti-obesity drugs a research hotspot.
Sedum heptose (α-D-altro-3-Heptulofuranose, CAS No.: 25545-06-6), as an emerging natural product, has attracted widespread attention due to its unique chemical structure and excellent pharmacological properties. In recent years, more and more studies have shown that Crassuance ketose has significant biological activity in regulating lipid metabolism, energy balance, and inflammatory responses, especially showing potential value in the anti-obesity field. This paper will systematically review the chemical structure and physicochemical properties of Crassuance heptose, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and pharmacokinetic characteristics, and explore its clinical application prospects and future development directions.
Crassulace ketose is a hepta-carbon sugar compound with the chemical name α-D-altro-3-Heptulofuranose, molecular formula C7H14O7, and molecular weight 210.1820. Its structural feature is a seven-carbon backbone form of furanose, containing multiple hydroxyl and ketone groups, giving it high polarity and water solubility. The LogP value of this compound was -2.6171, indicating strong hydrophilicity and difficulty in free diffusion through lipid membranes, suggesting that its distribution in vivo may favor aqueous environments. The total polar surface area (TPSA) was 130.6100 Ų, further supporting its good water solubility (216.0623 mg/mL), which is positive for the solubility and bioavailability of oral formulations.
The molecular structure of Crasulace ketose does not contain aromatic rings or long-chain fat groups, and it lacks obvious hydrophobic regions, which means its metabolic pathways in the body may mainly depend on enzyme systems related to carbohydrate metabolism. Additionally, its low blood-brain barrier permeability suggests that the compound has difficulty entering the central nervous system, reducing the risk of side effects. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames mutagenic test result was 0.0, indicating extremely low genotoxicity risk and meeting basic requirements for safe medication.
Crassuance heptose is mainly found in various Crassulaceae plants, especially abundant in Sedum spp. and related succulents. Traditional medicinal plants such as Sedum sarmentosum and Echidum (Dudleya spp.) have been widely reported to contain such heptacans derivatives. Its biosynthetic pathway may be closely related to carbohydrate metabolism within plants, serving as intermediate metabolites in energy metabolism and stress resistance.
Common methods for extracting ketose from Crassuance include water extraction, alcohol extraction, and their combined processes. Due to its high hydrophilicity, water extraction is usually preferred, and combining it with ultrasound-assisted extraction technology can improve extraction efficiency. After concentration and freeze-drying, the extract is purified and identified using high-performance liquid chromatography (HPLC) or GC-MS technology. In recent years, the application of ion exchange resins and membrane separation technologies has further improved the purity and recovery rate of Crassuance heptantose.
In addition, biosynthesis and microbial fermentation technologies have provided new ideas for the large-scale production of Jingtian heptose. By genetically engineering related enzyme strains to increase the yield and purity of heptacans, it is expected to meet both clinical and industrial needs.
Sedum heptose shows multi-target and multi-mechanism comprehensive regulatory effects in anti-obesity research. Both in vitro cell models and animal experiments have shown that it can significantly inhibit adipocyte differentiation and lipid accumulation, promote fatty acid β-oxidation, and regulate energy metabolism balance.
In a high-fat diet-induced obese mouse model, Crassuance ketose significantly reduced the rate of weight gain, decreased adipose tissue mass, improved abnormal blood lipid profiles, and lowered serum triglycerides and LDL cholesterol levels. In addition, it can improve insulin resistance and enhance glucose tolerance, demonstrating promising potential for preventing and treating metabolic syndrome.
Obesity is accompanied by chronic low-grade inflammation. Crassuance heptose reduces adipose tissue inflammation by regulating inflammatory factor expression. Studies have found that it can downregulate the expression of pro-inflammatory cytokines TNF-α and IL-6, inhibit M1 polarization in macrophages, and promote the transformation of the M2 anti-inflammatory phenotype, thereby improving the adipose tissue microenvironment.
In addition, ketose also helps regulate hormones secreted by fat cells, such as leptin (LEP) and adiponectin (ADIPOQ), promoting energy metabolism and insulin sensitivity, further exerting anti-obesity and metabolic regulatory effects.
The anti-obesity effects of Crassuance ketose involve several key molecular targets, mainly including:
PPARG (Peroxisome Proliferator-Activated Receptor γ): As a core regulator of adipocyte differentiation, Crassuance heptose inhibits adipocyte formation and lipid accumulation by modulating PPARG expression levels.
SREBF1 (sterol regulatory factor-binding protein 1): This transcription factor regulates genes related to fatty acid synthesis. Jingtian heptose downregulates SREBF1 expression, reducing the activity of fatty acid synthase (FASN) and lowering lipid synthesis.
LEPR (leptin receptor) and LEP (leptin): Crassuance ketose regulates leptin and its receptor expression, improving energy balance and appetite control.
ADRB3 (β3 adrenergic receptor) and UCP1 (uncoupled protein 1): promote calorie consumption and non-trembling thermogenesis in brown adipose tissue, enhancing energy expenditure.
FABP4 (fatty acid-binding protein 4): Regulates fatty acid transport and metabolism. Crassuance heptose ketose promotes fatty acid metabolism and utilization by regulating FABP4 expression.
ADIPOQ (adiponectin) and POMC (melanocyte-stimulating cells): involved in regulating insulin sensitivity and appetite; Jingtianheptose raises adiponectin levels and improves insulin resistance.
Through the synergistic effect of these multiple targets, Jingtian heptose ketose effectively regulates lipid metabolism, energy expenditure, and inflammatory response, exerting a comprehensive anti-obesity effect.
The druggability parameters of Jingtianheptose show good safety and drug development potential. Its low LogP and high TPSA value suggest that oral absorption may be limited, but good water solubility aids formulation design. The blood-brain barrier has low permeability, reducing the risk of central nervous system side effects. hERG channel inhibition is negative, and Ames tests show no mutagenicity, indicating low risks of cardiotoxicity and genotoxicity.
Pharmacokinetic studies show that ketose is mainly excreted in the body via the kidneys, has a moderate half-life, and its bioavailability is limited by its hydrophilicity and molecular size. The metabolic pathway mainly involves carbohydrate-related enzymes, and no significant hepatotoxic metabolites have been found. In the future, structural modification and drug carrier technologies can further optimize their pharmacokinetic characteristics, improving in vivo stability and targeting.
As a naturally derived anti-obesity active compound, Sedum heptose shows good pharmacological activity and safety, showing potential as a novel anti-obesity drug. Its multi-target mechanism meets the complex pathology needs of obesity and is expected to overcome the limitations of traditional single-target drugs.
Future research should focus on:
Preclinical safety and toxicological assessment: Systematically assessing the safety of long-term medication to lay the foundation for clinical trials.
Dosage form development and drug route optimization: Combining nanocarriers, sustained-release formulations, and other technologies to improve bioavailability and targeting.
Clinical trial design: Conduct multicenter, randomized, double-blind clinical trials to verify its anti-obesity effects and metabolic syndrome improvement.
Combination medication strategies: Explore synergistic effects with existing anti-obesity drugs or lifestyle interventions to enhance treatment outcomes.
In-depth Molecular Mechanisms: Using multi-omics techniques such as genomics and metabolomics to reveal their networks of action and potential new targets.
In summary, Jingtianheptose has promising prospects as a safe and effective anti-obesity drug and deserves further in-depth development and clinical translation.
As a natural product with a unique structure and significant anti-obesity activity, Jingtianheptose ketose demonstrates broad drug development potential through its multi-target regulation mechanism of lipid metabolism, energy balance, and inflammatory response. Its excellent safety and druggability parameters provide a solid foundation for clinical application. In the future, through systematic pharmacological mechanism research, pharmacokinetic optimization, and clinical validation, Jingtian Heptose is expected to become a new natural drug for anti-obesity and related metabolic disease treatment, providing new solutions for global obesity prevention and control.
Shenshuai
Wenjing
Hedandan
