Product name: Salidroside
Synonym name: Rhodosin; Rhodioloside
Catalogue No.: BP1246
Cas No.: 10338-51-9
Formula: C₁₄H₂₀O₇
Mol Weight: 300.307
Botanical Source: Rhodiolae Crenulatae Radixet Rhizoma
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

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.

​Description:

Salidroside is a prolyl endopeptidase inhibitor, which has cardioprotective, antidiabetic,antidepressant, anxiolytic, anti-tumor, and antioxidant actions. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling. It alleviates the pulmonary symptoms of paraquat-induced acute lung injury, at least partially, by repressing inflammatory cell infiltration and the expression of TGF-β1 resulting in delayed lung fibrosis; and it has protective effect against hypoxia-induced cardiomyocytes necrosis and apoptosis by increasing HIF-1α expression and subsequently up-regulating VEGF levels. It may be a potential therapeutic agent for treating or preventing neurodegenerative diseases implicated with oxidative stress.

References:

Int J Clin Exp Pathol. 2015 Jan 1;8(1):615-21. eCollection 2015.    

Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway.    

Salidroside is considered to have anti-tumor properties. We investigate its effects on colon carcinoma SW1116 cells. 

METHODS AND RESULTS:

Cell viability was assessed by CCK-8. Propidium iodide (PI) staining was used to determine the cell cycle by flow cytometry. The migration and invasion were detected by Transwell. Western blot was used to detect the expression of STAT3 signal related proteins. As the result, high concentrations of Salidroside (10, 20. 50 μg/ml) significantly inhibited proliferation of SW1116 cells in a parallelly, cell cycle arrest was increased at the G0/G1 phase after Salidroside treatment. Furthermore, Salidroside inhibited migration and invasion of SW1116 cells. Salidroside treatment decreased proteins expression of phosphorylation levels in JAK2/STAT3 signaling, while MMP-2 and MMP-9 proteins levels were decreased and protein expression of VEGF and VEGFR-2 were down-regulated. 

CONCLUSIONS:

In Conclusion, Salidroside inhibited proliferation, decreased the migration and invasion of SW1116 cells in JAK2/STAT3-dependent pathway, the specific mechanisms need further study.    

Br J Pharmacol. 2015 Mar 5.    

Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3β pathway.    

Recent reports have suggested that Salidroside could protect cardiomyocytes from oxidative injury and stimulate glucose uptake in skeletal muscle cells by activating AMP-activated protein kinase (AMPK). The aim of this study was to evaluate the therapeutic effects of Salidroside on diabetic mice and to explore the underlying mechanisms. 

METHODS AND RESULTS:

The therapeutic effects of Salidroside on type 2 diabetes were investigated. Increasing doses of Salidroside (25, 50 and 100 mg·kg(-1) ·day(-1)) were administered p.o. to db/db mice for 8 weeks. Biochemical analysis and histopathological examinations were conducted to evaluate the therapeutic effects of Salidroside. Primary cultured mouse hepatocytes were used to further explore the underlying mechanisms in vitro. Salidroside dramatically reduced blood glucose and serum insulin levels and alleviated insulin resistance. Hypolipidaemic effects and amelioration of liver steatosis were observed after Salidroside administration. In vitro, Salidroside dose-dependently induced an increase in the phosphorylations of AMPK and PI3K/Akt, as well as glycogen synthase kinase 3β (GSK3β) in hepatocytes. Furthermore, Salidroside-stimulated AMPK activation was found to suppress the expression of PEPCK and glucose-6-phosphatase. Salidroside-induced AMPK activation also resulted in phosphorylation of acetyl CoA carboxylase, which can reduce lipid accumulation in peripheral tissues. In isolated mitochondria, Salidroside inhibited respiratory chain complex I and disturbed oxidation/phosphorylation coupling and moderately depolarized the mitochondrial membrane potential, resulting in a transient increase in the AMP/ATP ratio. 

CONCLUSIONS:

Salidroside exerts an antidiabetic effect by improving the cellular metabolic flux through the activation of a mitochondria-related AMPK/PI3K/Akt/GSK3β pathway.    

J Surg Res. 2015 Jan 14. pii: S0022-4804(15)00057-8.    

Salidroside rescued mice from experimental sepsis through anti-inflammatory and anti-apoptosis effects.   

Salidroside (SDS) is the main effective component of Rhodiola rosea L with a variety of pharmacologic properties. The objective of this study was to investigate the efficacy of SDS in the treatment of experimental sepsis in mice and explore the possible underlying action mechanisms. 

METHODS AND RESULTS:

Sepsis was induced in C57BL/6 male mice via cecal ligation and puncture (CLP). The animals were divided into three groups as follows: sham, CLP, and CLP plus SDS. SDS (50 mg/kg) was injected intraperitoneally 1 h after operation. Postoperative survival of the mice, bacterial clearance in blood and peritoneal lavage fluid, cytokine secretion in blood, and histology of lung were evaluated. In addition, apoptosis of immune cells in the spleen and thymus were examined, respectively. SDS administration prolonged the survival of the septic mice, inhibited the proinflammatory responses, and enhanced bacterial clearance. It also alleviated the pathologic changes in the lung and inhibited the apoptosis of immune cells in the spleen and thymus after CLP challenge. 

CONCLUSIONS:

SDS exerts a protective effect in CLP-induced sepsis by attenuating the proinflammatory responses, enhancing bacterial clearance, and preserving adaptive immunity. SDS may be a promising therapeutic strategy for the treatment of sepsis.    

Behav. Brain Res., 2013, 244(244):70–81.    

Salidroside attenuates beta amyloid-induced cognitive deficits via modulating oxidative stress and inflammatory mediators in rat hippocampus.   

Beta amyloid (Aβ)-induced oxidative stress and chronic inflammation in the brain are considered to be responsible for the pathogenesis of Alzheimer's disease (AD). Salidroside, the major active ingredient of Rhodiola crenulata, has been previously shown to have antioxidant and neuroprotective properties in vitro. The present study aimed to investigate the protective effects of Salidrosideon Aβ-induced cognitive impairment in vivo. 

METHODS AND RESULTS:

Rats received intrahippocampal Aβ1-40 injection were treated with Salidroside (25, 50 and 75 mg/kg p.o.) once daily for 21 days. Learning and memory performance were assessed in the Morris water maze (days 17-21). After behavioral testing, the rats were sacrificed and hippocampi were removed for biochemical assays (reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA), acetylcholinesterase (AChE), acetylcholine (ACh)) and molecular biological analysis (Cu/Zn-SOD, Mn-SOD, GPx, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, nuclear factor κB (NF-κB), inhibitor of κB-alpha (IκBα), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), receptor for advanced glycation end products (RAGE)). Our results confirmed that Aβ1-40 peptide caused learning and memory deficits in rats. Further analysis demonstrated that the NADPH oxidase-mediated oxidative stress was increased in Aβ1-40-injected rats. Furthermore, NF-κB was demonstrated to be activated in Aβ1-40-injected rats, and the COX-2, iNOS and RAGE expression were also induced by Aβ1-40. However, Salidroside (50 and 75 mg/kg p.o.) reversed all the former alterations. 

CONCLUSIONS:

Thus, the study indicates that Salidroside may have a protective effect against AD via modulating oxidative stress and inflammatory mediators.    

HPLC of Salidroside

HNMR of Salidroside

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

Introduction/Overview

Salidroside (CAS No.: 10338-51-9) is an active natural compound isolated from plants of the Rhodiola genus, classified as a glycoside compound. As one of the main bioactive components in Rhodiola rosea, salidiola glycosides have attracted attention for their diverse pharmacological activities, especially showing significant potential in anti-fatigue, neuroprotection, anti-tumor, and metabolic regulation. In recent years, with in-depth research into its molecular mechanisms, its role in regulating cellular energy metabolism, mitochondrial function, and signal transduction pathways has become clearer, demonstrating its unique value as a novel natural drug molecule.

This paper will systematically review the chemical structure and physicochemical properties of salidroside (salidroside), plant origin, and extraction methods, with a focus on its pharmacological activity and mechanism of action. Combined with the latest molecular target studies, it will explore its druggability and pharmacokinetic characteristics, and finally look ahead to its prospects and challenges in clinical application, aiming to provide a comprehensive theoretical foundation and research reference for the fields of natural product pharmacology and new drug development.

Chemical structure and physicochemical properties

The chemical name of salidroside is 4-(β-D-pyranglucosy)phenylethanol, with the molecular formula C14H20O7 and a molecular weight of 300.3070. Its structure consists of a phenylethanol group connecting a glucose molecule via β-glycosidic bonds, making it a glycoside compound. The LogP value of salidroside is -0.4086, indicating strong hydrophilicity. Its water solubility is 9.0354, indicating good water solubility, which is beneficial for absorption and distribution in the body.

The polar surface area (TPSA) of salidroside is 119.6100 Ų, suggesting that its molecules have high polarity and a number of hydrogen bond donors/acceptors, affecting their ability to cross cell membranes. Its low blood-brain barrier permeability indicates that its distribution in the central nervous system is limited, but it can still exert neuroprotective effects by modulating the peripheral nervous system and indirectly through indirect mechanisms. The hERG channel inhibition test was negative, indicating a low risk of salidroside cardiotoxicity. The Ames mutagenic test result was 0.0, indicating no significant genotoxicity.

Plant Origins and Extraction Methods

Salidiola glycosides are mainly found in Rhodiola species, with the highest content in the rhizomes of Rhodiola rosea. Rhodiola is a perennial herbaceous plant widely distributed in cold and cold temperate regions, with a long medicinal history. Its rhizomes contain abundant glycosides, phenols, and volatile oils, with salidroside being the most representative active component.

There are various methods for extracting salidroside. Traditionally, water or ethanol extraction is used, combined with ultrasound-assisted extraction technology to improve extraction efficiency. Common steps include: crushing the dried Rhodiola rhizome, reflux extraction with 50%-70% ethanol aqueous solution, followed by filtrate concentration, precipitation, and column chromatography purification to obtain high-purity salidioside salidioside. In recent years, supercritical CO2 extraction and membrane separation technologies have also been introduced to achieve green and efficient extraction processes.

Pharmacological activity research

Salidroside shows significant effects in various biological activities, mainly including anti-fatigue, neuroprotection, anti-tumor, and metabolic regulation.

1. Anti-fatigue effects
   Salidroside can significantly enhance the body's endurance and resistance to fatigue. Animal experiments have shown that salidioside promotes fatty acid oxidation and mitochondrial function by regulating energy metabolism-related targets such as AMPK, SIRT1, and PPARG, thereby delaying the onset of fatigue. In addition, salidroside affects the neurotransmitter system, regulates targets such as MAOA, SLC6A4, ADRB2, and HTR1A, improves central nervous system function, and enhances mental status and cognitive abilities.

2. Neuroprotective effects
   Salidroside protects dopaminergic neurons from oxidative stress and apoptosis damage by enhancing PINK1/Parkin-mediated mitophagy, demonstrating potential therapeutic value for neurodegenerative diseases such as Parkinson's. In addition, its antioxidant and anti-inflammatory effects help reduce nerve damage and promote nerve repair.

3. Antitumor and alleviation of cachexia
   As a prolyl endopeptidase (PEP) inhibitor, salidroside can alleviate cachexia symptoms in tumor cachexia mouse models by activating the mTOR signaling pathway, improving weight loss and muscle atrophy. Its ability to regulate cellular metabolism and the immune microenvironment offers new ideas for adjuvant cancer therapy.

4. Other pharmacological effects
   Salidioside also exhibits multiple activities including anti-inflammatory, antioxidant, cardiovascular protection, and immune regulation, involving multiple signaling pathways and molecular targets, demonstrating its broad pharmacological potential.

Mechanism of action and molecular targets

The multi-target mechanism of salidroside is the basis for its pharmacological diversity. The main targets and signaling pathways involved are as follows:

1. AMPK（5' AMP-activated protein kinase）
   As a key regulator of cellular energy metabolism, AMPK activation promotes fatty acid oxidation and glucose metabolism. Salidroside improves energy metabolism imbalance by activating AMPK, enhancing the body's resistance to fatigue.

2. SIRT1 (Silent Information Regulatory Factor 2-Related Enzyme 1)
   SIRT1 is involved in regulating cellular stress responses and metabolic homeostasis. Salidroside promotes mitochondrial biogenesis and antioxidant reactions by activating SIRT1, protecting nerve cell function.

3. PPARG (Peroxisome Proliferator-Activated Receptor γ)
   PPARG regulates lipid metabolism and inflammatory responses, while salidroside improves lipid metabolism disorders and inflammatory states by modulating PPARG expression.

4. PINK1/Parkin-mediated mitophagy
   Salidiola enhances the PINK1/Parkin signaling pathway, promotes clearance of damaged mitochondria, maintains mitochondrial quality control, and protects dopaminergic neurons from damage.

5. mTOR signaling pathway
   Salidroside activates mTOR signaling, regulates protein synthesis and cellular metabolism, alleviating muscle atrophy and weight loss related to tumor cachexia.

6. Neurotransmitter-related targets
   Salidroside regulates targets such as MAOA (monoamine oxidase A), SLC6A4 (serotonin transporter), ADRB2 (β2 adrenergic receptor), and HTR1A (serotonin receptor 1A), improving neurotransmitter balance and enhancing central nervous system function.

7. UCP1 (uncoupling protein 1) and CREB1/BDNF signaling
   Salidroside promotes thermogenesis and energy expenditure by regulating UCP1, activates CREB1 and BDNF signaling, and enhances neuroplasticity and cognitive function.

Druggability evaluation and pharmacokinetics

The druggability evaluation of salidroside shows it has good safety and efficacy potential. It has a moderate molecular weight (300.3070) and good water solubility (9.0354), which is beneficial for oral absorption. The LogP value is -0.4086, indicating strong hydrophilicity, which may limit cell membrane permeability but contributes to solubility in blood circulation.

The low permeability of the blood-brain barrier suggests that salidroside has limited direct effects on the central nervous system, but it can still exert neuroprotective effects by modulating peripheral nerves and indirect mechanisms. The hERG suppression test was negative, indicating a low risk of cardiotoxicity. The Ames test is non-mutagenic and has relatively high safety.

Pharmacokinetic studies show that salidroside is rapidly absorbed in the body after oral administration, with a moderate plasma half-life, mainly metabolized by the liver and excreted by the kidneys. Most of its metabolites are in deglycosylated form, with some having biological activity. The bioavailability of salidroside is affected by intestinal enzymatic lysis and first-pass effects. Future formulation improvements and delivery route optimization are expected to enhance its clinical value.

Prospects and outlooks for clinical applications

As a versatile natural product, salidroside has broad clinical application potential. Its anti-fatigue effects are suitable for sports medicine and adjunctive treatment of chronic fatigue syndrome; Neuroprotective effects provide new therapeutic strategies for neurodegenerative diseases such as Parkinson's and Alzheimer's; The antitumor and cachexia-alleviating effects support the comprehensive management of cancer patients.

Currently, salidroside is still in the early stages of clinical research, facing challenges such as dose optimization, administration methods, and long-term safety evaluation. In the future, in-depth analysis of its pharmacological mechanisms should be strengthened, combined with modern medicinal chemistry and pharmaceutics techniques to develop efficient and safe salidioside derivatives and compound formulations. At the same time, large-scale, multicenter clinical trials are being conducted to verify efficacy and safety, laying a solid foundation for its transformation into commonly used clinical drugs.

In addition, the potential applications of salidroside in metabolic diseases, immune regulation, and neuropsychiatric disorders are also worth further exploration. By combining precision medicine with molecular targeted therapy concepts, salidroside is expected to become a key breakthrough in the development of natural product drugs.

Conclusion

As the main active ingredient in Rhodiola, salidioside demonstrates broad biological activity and good druggability due to its unique chemical structure and multi-target pharmacological effects. Its research progress in anti-fatigue, neuroprotection, and alleviation of tumor cachexia provides valuable scientific evidence for natural product pharmacology and new drug development.

In the future, as molecular mechanisms continue to be revealed and clinical research deepens, salidroside is expected to become a novel natural drug for treating various diseases. Strengthening its pharmacokinetic optimization and safety evaluation will promote its clinical application and promote the widespread use of natural products in modern medicine.