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Fig. 1 · Structure
Cat. No.
A12043
CAS No.
490-46-0
Formula
C15H14O6
Mol. Weight
290.27

Documents & Downloads

(-)-Epicatechin

Cat. No. A12043 CAS 490-46-0

COX-1 inhibitor

(-)-Epicatechin is a natural product from green tea. (-)Epicatechin is an inhibitor of Cox-1

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Publications for (-)-Epicatechin

5 publications citing this product

  1. Grace Northrop, .et al. , Food Funct, 2022, Apr 4;13(7):3894-3904 PMID: 35285840
  2. A S D'Costa, .et al. , Food Chem, 2020, Oct 1;341(Pt 2):128256 PMID: 33035827
  3. Mihaela Tudorache, .et al. , Food Hydrocoll, 2019, 97, Dec, 105193
  4. Md Shajedul Islam, .et al. , Innovative food science & emerging technologies, 2016, v.34 pp. 344-351
  5. Islam MS, .et al. , J Agric Food Chem, 2016, Oct 10 PMID: 27632812
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Biological Activity

Bioactivity / Mechanism

(-)-Epicatechin elicited a partially calcium-independent NO response in cultured human coronary artery endothelial cells. Under calcium-depleted conditions, increased eNOS Ser-1177, Ser-633 and Ser-615 phosphorylation accompanied the response, while Thr-495 phosphorylation was unchanged. These cellular observations support eNOS-related signaling; they do not identify a directly bound molecular target. [1]

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

Target & Activity

Target Activity Value
COX-1 IC50 3.2 μM

Cellular Effect

Cell Line Activity Value Description Reference
A549 ED50 > 10 μg/mL Cytotoxicity against human A549 cells by tetrazolium salt-based colorimetric assay [PMID: 1431932]
BMDC IC50 > 50 μM Inhibition of LPS-induced IL-12 p40 production in wild-type C57BL/6 mouse BMDC pretreated with compound for 1 hr before LPS treatment measured 16 hrs by ELISA [PMID: 25769817]
BMDC IC50 > 50 μM Inhibition of LPS-induced IL-6 production in wild-type C57BL/6 mouse BMDC pretreated with compound for 1 hr before LPS treatment measured 16 hrs by ELISA [PMID: 25769817]
BMDC IC50 > 50 μM Inhibition of LPS-induced TNF-alpha production in wild-type C57BL/6 mouse BMDC pretreated with compound for 1 hr before LPS treatment measured 16 hrs by ELISA [PMID: 25769817]
BV-2 IC50 47.37 μM Antineuroinflammatory activity in human BV2 cells assessed as inhibition of LPS-induced NO production after 24 hrs in presence of LPS by Griess reaction [PMID: 27623545]
HCT-8 ED50 > 10 μg/mL Cytotoxicity against human HCT8 cells by tetrazolium salt-based colorimetric assay [PMID: 1431932]
KB ED50 > 10 μg/mL Cytotoxicity against human KB cells by tetrazolium salt-based colorimetric assay [PMID: 1431932]
L929 EC50 300 μM Inhibition of recombinant human TNF-alpha-induced cytotoxicity of mouse L929 cells assessed as survivality preincubated for 15 mins before TNFalpha addition measured after 24 hrs by crystal violet staining [PMID: 9287415]
L929 EC50 350 μM Inhibition of recombinant human TNF-alpha-induced cytotoxicity of mouse L929 cells assessed as survivality preincubated for 15 mins before TNFalpha addition measured after 24 hrs by [methyl-3H]thymidine incorporation assay [PMID: 9287415]
LNCaP EC50 13 μM Decrease in androgen receptor protein expression in LNCaP cells by Western blotting [PMID: 17383188]
MT4 CC50 136.2 μg/mL Cytotoxicity against human MT4 cells by MTT assay [PMID: 10425115]
MT4 IC50 34.1 μg/mL Antiviral activity against HIV infected in human MT4 cells assessed as inhibition of virus-induced cytopathic effect by MTT assay [PMID: 10425115]
PC-3 IC50 > 500 μM In vitro inhibitory concentration against PC-3 cell line in MTT assay was determined after 3 days incubation [PMID: 15380225]
Platelet IC50 > 50 μg/mL Antiaggregatory activity in human platelets assessed as inhibition of thrombin-induced platelet aggregation by aggregometry [PMID: 21106454]
Platelet IC50 22.22 μg/mL Antiaggregatory activity in human platelets assessed as inhibition of collagen-induced platelet aggregation by aggregometry [PMID: 21106454]
SK-OV-3 IC50 > 500 μM In vitro inhibitory concentration against SKOV3 cell line in MTT assay was determined after 3 days incubation [PMID: 15380225]
TE-671 ED50 > 10 μg/mL Cytotoxicity against human TE671 cells by tetrazolium salt-based colorimetric assay [PMID: 1431932]
U-373MG ATCC IC50 > 500 μM In vitro inhibitory concentration against U373MG cell line in MTT assay was determined after 3 days incubation [PMID: 15380225]
Vero IC50 184.1 μM Cytotoxicity against african green monkey Vero cells after 4 hrs by MTT assay [PMID: 16724851]

19 records · Scroll to view more

In Vitro Studies

In human coronary artery endothelial cells, (-)-epicatechin increased an indirect extracellular NO endpoint across 0.1 nmol/l–1 μmol/l. Calcium depletion retained approximately 25% of the regular-calcium response, whereas the bradykinin response was abolished. Media were sampled after 10 min. Calcium-green fluorescence verified the loss of the stimulus-induced calcium rise. [1]

Endothelial NO response and eNOS phosphorylation during calcium depletion

Cell-based study · Human coronary artery endothelial cells from healthy male donors (14, 40 and 60 years); passages 12–14; regular-calcium and calcium-depleted conditions. [1]

EPI retained a partial NO-related response after calcium depletion, whereas bradykinin did not. This was accompanied by eNOS serine phosphorylation, with no change in Thr-495. These are cellular signaling results; physiological relevance was not established.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Indirect extracellular NO response after calcium depletionreported outcome Approximately 25% of the response in regular-calcium conditions remained with EPI; bradykinin-induced NO response was abolished. Figure 1 reports means ± SD, n = 3; Data analysis states a minimum of three experiments, each in triplicate unless noted.[1]
eNOS phosphorylation under calcium-depleted conditionsreported outcome Ser-1177, Ser-633 and Ser-615 phosphorylation increased relative to unstimulated control; Thr-495 phosphorylation did not change. Means ± SD, n = 3; caption reports t-test, P < 0.05 for increases.[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.1 nmol/l–1 μmol/l for NO/calcium concentration responses; 1 μmol/l for the calcium-depletion comparison and Figure 2 immunoblots.
Exposure duration
10 min for collection of media for NO measurements; calcium kinetics assessed over 0–10 s.
Method
Cells treated with EPI under regular or experimentally depleted calcium conditions. Calcium green fluorescence verified loss of the stimulus-induced calcium response; culture-media nitrite/nitrate fluorometry was used as an indirect NO endpoint.
Vehicle
Water for EPI; DMSO for bradykinin, with corresponding vehicle controls.
Co-treatment
Bradykinin was a separate comparator, not combined therapy. Amlodipine was a separate positive control for eNOS Ser-1177 phosphorylation.
Reported limits
A separate EPI exposure time for Figure 2 immunoblots and the amlodipine concentration are not specified in the relevant main-text methods/caption; not inferred from the NO assay. Purity/lot and analytical stereochemical verification are not reported in Materials.
Methods and source locations

Compound reported in the paper: (-)-Epicatechin; Compound label in the paper: EPI

Evidence for the reported (-)-epicatechin material and model; no validation of Adooq A12043 lots or clinical efficacy.

Methods: Materials, Cell culture, [Ca2+]i measurements, NO measurements, Immunoblotting, Data analysis; Results and Figures 1–2

Indirect extracellular NO response after calcium depletion: Nitrite/nitrate fluorometric assay of culture media; calcium-green fluorescence as calcium-depletion control. — Methods: NO measurements and Data analysis; Results: EPI-induced NO production is partially Ca2+ independent; Figure 1A–C and caption

eNOS phosphorylation under calcium-depleted conditions: Immunoblotting; total eNOS normalization; amlodipine positive control for Ser-1177. — Methods: Immunoblotting; Results: EPI induces phosphorylation of eNOS amino acid activation residues under Ca2+-free conditions; Figure 2 and caption

In Vivo Studies

In one-year-old male mice, 15 days of oral (-)-epicatechin increased treadmill performance relative to water controls; adding the tested exercise regimen did not significantly increase treadmill indices beyond epicatechin alone. In a separate healthy young-adult rat study using a different dose and assessment schedule, endurance capacity and peak oxygen uptake did not improve significantly. The differing model-specific responses do not establish a general exercise-enhancing effect. [2,3]

In healthy male rats, oral (-)-epicatechin lowered mean arterial pressure at rest and during submaximal exercise. Total exercising hindlimb blood flow and vascular conductance were not significantly changed, although vascular conductance increased in five individual muscles or muscle parts. These vascular outcomes do not establish that the cellular eNOS pathway caused the in vivo response. [3]

Fifteen-day mouse treadmill performance study

Animal study · One-year-old male C57BL/6N mice; 25 randomized to water (n = 6), water plus exercise (n = 7), EPI (n = 5), or EPI plus exercise (n = 7). [2]

At Day 15, both EPI groups had greater treadmill performance than the water groups. Added exercise did not significantly improve treadmill indices relative to EPI alone. Body and sampled heart/muscle masses did not differ significantly among groups.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Incremental treadmill running duration at Day 15reported outcome Water 730 ± 29 s (n = 6); water-exercise 745 ± 27 s (n = 7); EPI 931 ± 32 s (n = 5); EPI-exercise 958 ± 27 s (n = 7). Means ± SEM; each EPI group P < 0.05 vs water-only and water-exercise groups.[2]
Added-exercise and mass outcomesreported outcome No statistically significant treadmill-index difference between EPI alone and EPI plus exercise. No significant difference among groups for body, heart or hindlimb muscle mass indices (P > 0.05).[2]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Twice daily, morning and evening
Vehicle
Water
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
EPI alone
1.0 mg (kg body mass)−1 per administration		Water-only group (n = 6)Day 15 duration 931 ± 32 s (mean ± SEM; n = 5), P < 0.05 vs both water groups.[2]
EPI plus treadmill exercise
1.0 mg (kg body mass)−1 per administration		Water-exercise (n = 7), water only (n = 6), and EPI alone (n = 5)Day 15 duration 958 ± 27 s (mean ± SEM; n = 7), P < 0.05 vs both water groups; no significant treadmill-index difference from EPI alone.[2]
EPI alone
Model: One-year-old male C57BL/6N mice; 25 randomized to water (n = 6), water plus exercise (n = 7), EPI (n = 5), or EPI plus exercise (n = 7).
Treatment course: 15 consecutive days
EPI plus treadmill exercise
Model: One-year-old male C57BL/6N mice; 25 randomized to water (n = 6), water plus exercise (n = 7), EPI (n = 5), or EPI plus exercise (n = 7).
Treatment course: 15 consecutive days; treadmill exercise 30 min, five times per week during intervention
Methods and source locations

Compound reported in the paper: (-)-Epicatechin; Compound label in the paper: (-)-Epi

Evidence for the reported (-)-epicatechin material and model; no validation of Adooq A12043 lots or clinical efficacy.

Methods: Animals and ethical approval, Experimental design and approach, (-)-Epicatechin administration, Incremental treadmill tests, Exercise intervention, Statistical analyses; Results and Tables 1–2

Incremental treadmill running duration at Day 15: Incremental treadmill test before and after the intervention; mixed factorial ANOVA with post hoc comparisons. — Table 2, Duration (s), Day 15 columns and *, ** footnotes; Results: Incremental treadmill test

Added-exercise and mass outcomes: Treadmill tests and tissue/body mass comparisons. — Results: Animals and Incremental treadmill test; Table 1 and footnote; Table 2

EPI alone · Methods: (-)-Epicatechin administration; Table 2

EPI plus treadmill exercise · Methods: Exercise intervention and (-)-Epicatechin administration; Table 2

Rat endurance and peak oxygen uptake tests

Animal study · Approximately four-month-old male Sprague-Dawley rats randomized to water or EPI (initial n = 12/group). Endurance analysis: control n = 12, EPI n = 10; peak oxygen uptake: n = 7/group. [3]

EPI did not significantly improve exercise endurance or peak oxygen uptake in healthy rats. These findings differ from the selected older-mouse experiment; species, age, dosing and test conditions also differed, and the cause of the different responses is unknown.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Posttreatment treadmill endurance capacityreported outcome Control 43.4 ± 2.3 min; EPI 36.8 ± 2.9 min; P = 0.06. Change from pretreatment: control −9.2 ± 3.0 min; EPI −8.6 ± 2.3 min; P = 0.86. Reported ± values; dispersion is not explicitly defined for these text-only endpoints; control n = 12, EPI n = 10.[3]
Peak oxygen uptakereported outcome Control 84 ± 2; EPI 82 ± 4 ml·kg−1·min−1; P = 0.70. Reported ± values; dispersion is not explicitly defined for these text-only endpoints; n = 7/group.[3]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Twice daily, morning/afternoon
Treatment course
21 days before performance testing; dosing continued during assessment days; 24 days total by final vascular protocols
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
EPI performance group
2 mg/kg per administration (4 mg·kg−1·day−1 total)		Water-gavaged control ratsNo significant improvement in endurance capacity or peak oxygen uptake.[3]
EPI performance group
Model: Approximately four-month-old male Sprague-Dawley rats randomized to water or EPI (initial n = 12/group). Endurance analysis: control n = 12, EPI n = 10; peak oxygen uptake: n = 7/group.
Reported limits: The EPI gavage vehicle is not explicitly specified in Animal Care and Assignment; control rats received water.
Methods and source locations

Compound reported in the paper: (-)-Epicatechin; Compound label in the paper: EPI

Evidence for the reported (-)-epicatechin material and model; no validation of Adooq A12043 lots or clinical efficacy.

Methods: Animal Care and Assignment, Assessment of Exercise Performance, Statistical Analysis; Results: Body Mass, Endurance Capacity, and V̇o2 Peak

Posttreatment treadmill endurance capacity: Progressive treadmill run to exhaustion; unpaired t-test. — Methods: Endurance capacity and Statistical Analysis; Results: Body Mass, Endurance Capacity, and V̇o2 Peak

Peak oxygen uptake: Maximal treadmill test with respiratory gas analysis; unpaired t-test. — Methods: V̇o2 peak and Statistical Analysis; Results: Body Mass, Endurance Capacity, and V̇o2 Peak

EPI performance group · Methods: Animal Care and Assignment, Assessment of Exercise Performance, Surgical Instrumentation; Results: Body Mass, Endurance Capacity, and V̇o2 Peak

Conscious-rat submaximal exercise vascular protocol

Animal study · Healthy young adult male Sprague-Dawley rats; Protocol 1, control n = 11 and EPI n = 11 for resting and submaximal-exercise vascular measurements. [3]

EPI lowered resting and exercising mean arterial pressure, but total hindlimb blood flow and vascular conductance did not differ significantly. Five of 28 individual muscle/muscle-part vascular-conductance measurements were higher during exercise. This protocol does not establish the molecular mechanism of the blood-pressure effect.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Mean arterial pressure at rest and during submaximal exercisereported outcome Lower with EPI vs control at rest (P = 0.03) and during exercise (P = 0.04). Means ± SE; n = 11/group.[3]
Total exercising hindlimb muscle blood flow and vascular conductancereported outcome Blood flow: control 154 ± 13; EPI 159 ± 8 ml·min−1·100 g−1 (P = 0.68). Vascular conductance: control 1.13 ± 0.10; EPI 1.24 ± 0.08 ml·min−1·100 g−1·mmHg−1 (P = 0.21). Means ± SE; n = 11/group.[3]
Regional exercising vascular conductancereported outcome Higher in 5 of 28 muscles or muscle parts with EPI (P < 0.05): tibialis posterior, red tibialis anterior, biceps femoris posterior, semitendinosus and gracilis. No significant exercising blood-flow difference in the 28 individual muscles/parts.[3]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Twice daily, morning/afternoon
Treatment course
24 days total by final vascular measurements
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
EPI vascular group
2 mg/kg per administration (4 mg·kg−1·day−1 total)		Water-gavaged controls (n = 11 for Protocol 1)MAP lower at rest and submaximal exercise; total hindlimb flow and conductance not significantly changed.[3]
EPI vascular group
Model: Healthy young adult male Sprague-Dawley rats; Protocol 1, control n = 11 and EPI n = 11 for resting and submaximal-exercise vascular measurements.
Reported limits: The EPI gavage vehicle is not explicitly specified in Animal Care and Assignment; control rats received water.
Methods and source locations

Compound reported in the paper: (-)-Epicatechin; Compound label in the paper: EPI

Evidence for the reported (-)-epicatechin material and model; no validation of Adooq A12043 lots or clinical efficacy.

Methods: Animal Care and Assignment, Surgical Instrumentation, Protocol 1, Statistical Analysis; Results: Protocol 1; Figures 1–2 and Table 2

Mean arterial pressure at rest and during submaximal exercise: Arterial catheter measurements in conscious rats, resting and exercising; mixed two-way ANOVA. — Results: Protocol 1, Blood gases, blood [lactate], MAP, and HR; Figure 1 top panel and caption

Total exercising hindlimb muscle blood flow and vascular conductance: Radiolabeled microspheres for blood flow; vascular conductance = blood flow/MAP. — Abstract; Methods: Protocol 1; Results: Blood flow and VC; Figure 2 and caption

Regional exercising vascular conductance: Regional microsphere blood-flow measurements and calculated vascular conductance. — Results: Protocol 1, Blood flow and VC; Table 2 and * footnote

EPI vascular group · Methods: Animal Care and Assignment, Surgical Instrumentation, Protocol 1; Figures 1–2

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 490-46-0
Applications COX-1 inhibitor
Formula C15H14O6
Molecular Weight 290.27
Synonyms (?)Epicatechin
SMILES
C1[C@H]([C@H](OC2=CC(=CC(=C21)O)O)C3=CC(=C(C=C3)O)O)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 52 mg/mL (179.14 mM)
Water Insoluble
Ethanol Insoluble

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] Ramirez-Sanchez I, Maya L, Ceballos G, et al. (-)-Epicatechin induces calcium and translocation independent eNOS activation in arterial endothelial cells. American journal of physiology. Cell physiology (2011). PMID: 21209365 DOI: 10.1152/ajpcell.00406.2010 Source material
  2. [2] Nogueira L, Ramirez-Sanchez I, Perkins GA, et al. (-)-Epicatechin enhances fatigue resistance and oxidative capacity in mouse muscle. The Journal of physiology (2011). PMID: 21788351 DOI: 10.1113/jphysiol.2011.209924 Source material
  3. [3] Copp SW, Inagaki T, White MJ, et al. (-)-Epicatechin administration and exercising skeletal muscle vascular control and microvascular oxygenation in healthy rats. American journal of physiology. Heart and circulatory physiology (2013). PMID: 23144313 DOI: 10.1152/ajpheart.00714.2012 Source material

Publications

5 publications citing this product

  1. Grace Northrop, .et al. , Food Funct, 2022, Apr 4;13(7):3894-3904 PMID: 35285840
  2. A S D'Costa, .et al. , Food Chem, 2020, Oct 1;341(Pt 2):128256 PMID: 33035827
  3. Mihaela Tudorache, .et al. , Food Hydrocoll, 2019, 97, Dec, 105193
  4. Md Shajedul Islam, .et al. , Innovative food science & emerging technologies, 2016, v.34 pp. 344-351
  5. Islam MS, .et al. , J Agric Food Chem, 2016, Oct 10 PMID: 27632812

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