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Fig. 1 · Structure
Cat. No.
A10821
CAS No.
10338-51-9
Formula
C14H20O7
Mol. Weight
300.3

Documents & Downloads

Salidroside (Rhodioloside)

Cat. No. A10821 CAS 10338-51-9
Salidroside (Rhodioloside) is a glucoside of tyrosol found in the plant Rhodiola rosea. It is thought to be one of the compounds responsible for the antidepressant and anxiolytic actions of this plant, along with rosavin.

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Biological Activity

Target & Activity

Target Activity Value
mTOR  

Cellular Effect

Cell Line Activity Value Description Reference
HeLa IC50 10.493 μM Antiproliferative activity against human HeLa cells assessed as inhibition of cell proliferation measured after 48 hrs by CCK-8 assay [PMID: 34978808]
MDA-MB-231 IC50 40 μM Anticancer activity against human MDA-MB-231 cells assessed as cell growth inhibition incubated for 24 hrs by MTT assay [PMID: 33650861]
PC-12 EC50 0.3 μM Neuroprotective activity against CoCl2-induced cytotoxicity in rat PC12 cells assessed as increase in cell viability pretreated with CoCl2 for 8 hrs followed by incubation with drug and measured after 24 hrs by MTT assay [PMID: 33097301]

In Vitro Studies

C2C12 myotubes were incubated in HBSS with or without Salidroside under nutrition deprivation. Salidroside alleviated myotube atrophy, as indicated by increased myotube diameter compared with the nutrition deprivation group. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Myotube Diameter During Nutrition Deprivation

Cell-based study · C2C12 myotubes [1]

C2C12 myotubes were incubated in HBSS with or without Salidroside. Compared with nutrition deprivation alone, Salidroside alleviated myotube atrophy, as indicated by increased myotube diameter.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
myotube diameterReported result Salidroside (Sal L: 40 μM, Sal M: 80 μM, Sal H: 160 μM): salidroside could alleviate myotube atrophy induced by nutrition deprivation, which was confirmed by the increased myotube diameter.[1]

Literature-Reported Treatment Conditions

Treatment concentration
40 μM, Sal M: 80 μM, Sal H: 160 μM
Exposure duration
12 h
Method
incubated in HBSS
Vehicle
amino acid-free and serum-free Hank’s balanced salt solution (HBSS; Gibco Company)
Co-treatment
Other interventions in this design: HBSS. Compound effect isolated by the comparison: HBSS for 12 h with or without the presence of salidroside.
Methods and source locations

Compound reported in the paper: Salidroside

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and Methods > Cell Culture and Treatments (S8); Materials and Methods > Immunofluorescence and Quantification of Myotubes (S23, S24); Results > Salidroside Alleviates Myotube Atrophy Induced by Nutrition Deprivation (S55, S57); Figure 1 legend (S112)

myotube diameter: myotube diameter; comparator: (nutrition deprivation) ND group — Results > Salidroside Alleviates Myotube Atrophy Induced by Nutrition Deprivation (S55, S57)

In Vivo Studies

Salidroside given with free access in distilled water did not affect body weight in leptin deficient (ob/ob) mice. In db/db mice, Salidroside administered orally by gavage protected against developing severe hyperglycemia compared with vehicle, with protection sustained during subsequent treatment. In C57BL/6J mice fed high fat diets, Salidroside given with free access in distilled water markedly decreased liver triglyceride content compared with vehicle. [2,3]

Body weight in leptin deficient mice

Animal study · 4-week old leptin deficient (ob/ob) mice [2]

Leptin deficient (ob/ob) mice received Salidroside with free access in distilled water. Body weight was unaffected compared with mice given distilled water.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
body weightReported result the body weight of ob/ob mice was not affected by salidroside[2]

Conditions shared by the study groups

Route
given to mice with free access
Treatment course
48 days
Vehicle
distilled water
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Salidroside 0.3 mg/mlmice given distilled waterthe body weight of ob/ob mice was not affected by salidroside[2]
Salidroside 0.3 mg/ml
Model: 4-week old leptin deficient (ob/ob) mice
Methods and source locations

Compound reported in the paper: Salidroside

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Effects of salidroside on body weight and food intake (S2); Results > Salidroside has minimal euglycemic effects in ob/ob mice (S74, S75); Methods > Mice (S89, S90, S92)

body weight: body weight; comparator: mice given distilled water — Results > Salidroside has minimal euglycemic effects in ob/ob mice (S75)

Salidroside 0.3 mg/ml · Results > Effects of salidroside on body weight and food intake (S2); Results > Salidroside has minimal euglycemic effects in ob/ob mice (S74, S75); Methods > Mice (S89, S92)

Fasting blood glucose in BKS.Cg-Dock7m +/+ Leprdb/J (db/db) mice (n = 16)

Animal study · BKS.Cg-Dock7m +/+ Leprdb/J (db/db) mice (n = 16) [3]

Model: BKS.Cg-Dock7m +/+ Leprdb/J (db/db) mice (n = 16). Treatment: 100 mg/kg/day. Result: after 21-day treatment, db/db mice were protected from developing severe hyperglycemia by salidroside and this effect was sustained in following days compared to vehicle db/db group.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Fasting blood glucoseReported result after 21-day treatment, db/db mice were protected from developing severe hyperglycemia by salidroside and this effect was sustained in following days compared to vehicle db/db group[3]

Conditions shared by the study groups

Route
orally by gavage
Treatment course
once a day for 5 weeks
Vehicle
saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Salidroside 100 mg/kg/dayvehicle db/db groupafter 21-day treatment, db/db mice were protected from developing severe hyperglycemia by salidroside and this effect was sustained in following days compared to vehicle db/db group[3]
Salidroside 100 mg/kg/day
Model: BKS.Cg-Dock7m +/+ Leprdb/J (db/db) mice (n = 16)
Methods and source locations

Compound reported in the paper: Salidroside

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and Methods > Animals and Experimental Design (S8, S9, S10, S11); Results > Salidroside Alleviated Hyperglycemia in db/db and HFD Mice (S71)

Fasting blood glucose: Fasting blood glucose; comparator: vehicle db/db group — Materials and Methods > Animals and Experimental Design (S11); Results > Salidroside Alleviated Hyperglycemia in db/db and HFD Mice (S71)

Salidroside 100 mg/kg/day · Materials and Methods > Animals and Experimental Design (S9); Results > Salidroside Alleviated Hyperglycemia in db/db and HFD Mice (S71)

Liver triglyceride content during high fat feeding

Animal study · 6-week old C57BL/6J mice [2]

In mice receiving high fat diets, Salidroside was provided with free access in distilled water. Liver triglyceride content was markedly decreased compared with vehicle-treated mice.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
triglyceride content in liverReported result The triglyceride content in liver was markedly decreased[2]

Conditions shared by the study groups

Route
given to mice with free access
Treatment course
48 days
Vehicle
distilled water
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Salidroside around 50 mg/kg/daymice given distilled waterThe triglyceride content in liver was markedly decreased[2]
Salidroside around 50 mg/kg/day
Model: 6-week old C57BL/6J mice
Methods and source locations

Compound reported in the paper: Salidroside

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Effects of salidroside on body weight and food intake (S2, S3, S4); Results > Salidroside administration attenuates lipid accumulation in liver (S15, S20); Methods > Mice (S88, S89, S90)

triglyceride content in liver: triglyceride content in liver; comparator: mice given distilled water — Results > Salidroside administration attenuates lipid accumulation in liver (S20)

Salidroside around 50 mg/kg/day · Results > Effects of salidroside on body weight and food intake (S2, S4); Results > Salidroside administration attenuates lipid accumulation in liver (S20); Methods > Mice (S89)

Specifications

Manufacturer Adooq Bioscience
CAS Number 10338-51-9
Formula C14H20O7
Molecular Weight 300.3
Synonyms Rhodioloside
SMILES
C1=CC(=CC=C1CCO[C@H]2[C@@H]([C@H]([C@@H]([C@H](O2)CO)O)O)O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 58 mg/mL (193.14 mM)
Water 58 mg/mL (193.14 mM)
Ethanol 4 mg/mL (13.32 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Huang Z, Fang Q, Ma W, et al. Skeletal Muscle Atrophy Was Alleviated by Salidroside Through Suppressing Oxidative Stress and Inflammation During Denervation. Front Pharmacol (2019). PMID: 31616291 DOI: 10.3389/fphar.2019.00997 Source material
  2. [2] Wang M, Luo L, Yao L, et al. Salidroside improves glucose homeostasis in obese mice by repressing inflammation in white adipose tissues and improving leptin sensitivity in hypothalamus. Sci Rep (2016). PMID: 27145908 DOI: 10.1038/srep25399 Source material
  3. [3] Ju L, Wen X, Wang C, et al. Salidroside, A Natural Antioxidant, Improves β-Cell Survival and Function via Activating AMPK Pathway. Front Pharmacol (2017). PMID: 29093682 DOI: 10.3389/fphar.2017.00749 Source material

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