Pachymic acid

CAS# 29070-92-6

Pachymic acid

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Chemical structure

Pachymic acid

3D structure

Chemical Properties of Pachymic acid

Cas No. 29070-92-6 SDF Download SDF
PubChem ID 316448 Appearance White powder
Formula C33H52O5 M.Wt 528.76
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms 3-O-Acetyltumulosic acid
Solubility DMSO : 7.14 mg/mL (13.50 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name 2-(3-acetyloxy-16-hydroxy-4,4,10,13,14-pentamethyl-2,3,5,6,7,11,12,15,16,17-decahydro-1H-cyclopenta[a]phenanthren-17-yl)-6-methyl-5-methylideneheptanoic acid
SMILES CC(C)C(=C)CCC(C1C(CC2(C1(CCC3=C2CCC4C3(CCC(C4(C)C)OC(=O)C)C)C)C)O)C(=O)O
Standard InChIKey VDYCLYGKCGVBHN-UHFFFAOYSA-N
Standard InChI InChI=1S/C33H52O5/c1-19(2)20(3)10-11-22(29(36)37)28-25(35)18-33(9)24-12-13-26-30(5,6)27(38-21(4)34)15-16-31(26,7)23(24)14-17-32(28,33)8/h19,22,25-28,35H,3,10-18H2,1-2,4-9H3,(H,36,37)
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Pachymic acid

The root of Wolfiporia cocos (Schw.) Ryv.

Biological Activity of Pachymic acid

DescriptionPachymic acid has sedative-hypnotic, cardioprotective,antioxidant, and anti-inflammatory activities, it has hypoglycemic activity ,can stimulate glucose uptake, GLUT4 gene expression and translocation, and promoting triglyceride accumulation in adipocytes. Pachymic acid may inhibit proliferation and invasion of ovarian carcinoma cell through decreasing β-catenin and COX-2 expression and increasing E-cadherin exprssion. Pachymic acid is suggested to prevent the complications of oral diseases such as inflammation and alveolar destruction of the oral cavity.
TargetsNrf2 | TNF-α | IL Receptor | NF-kB | HO-1 | COX | Caspase | ERK | p38MAPK | GLUT | PI3K | AMPK | Akt | GABA Receptor
In vitro

The antioxidant property of pachymic acid improves bone disturbance against AH plus-induced inflammation in MC-3T3 E1 cells.[Pubmed: 23522537]

J Endod. 2013 Apr;39(4):461-6.

The cytotoxicity of resin-based sealer is influential on the inflammatory reaction and cell survival for oral periapical cells. In this study, Pachymic acid as an antioxidant was investigated for the improvement of bone disturbance against AH Plus (Dentsply DeTrey GmbH, Konstanz, Germany)-induced inflammation in MC-3T3 E1 cells.
METHODS AND RESULTS:
AH Plus was prepared according to the manufacturer's instructions. Using mouse osteoblast cells (MC-3T3 E1), a specimen of AH Plus was eluted with the culture medium for 1 day and was diluted by 30%. The cellular cytotoxicity and reactive oxygen species formation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and 2',7'-dichlorodihydrofluorescein diacetate with fluorescence-activated cell sorting. The secretion of proinflammatory cytokines was determined by an enzyme-linked immunosorbent assay, and the expression of inflammatory and osteogenic molecules was determined by immunoblotting. Cells with AH Plus elutes showed a decrease of cell viability and ALP activity. However, Pachymic acid and N-acetyl-L-cysteine (control antioxidant) restored cell viability and ALP activity damaged by AH plus. The secretion of nitric oxide, tumor necrosis factor α, and interleukin-1β were increased in AH Plus-stimulated MC-3T3 E1 cells, but Pachymic acid suppressed its production. Furthermore, Pachymic acid reduced the receptor activator of nuclear factor-κB ligand, cyclooxygenase-2, matrix metalloproteinase-2 and -9, increased bone morphogenetic protein-2 and -7, and runt-related transcription factor 2 despite AH Plus stimuli. In addition, Pachymic acid affected the removal effect of reactive oxygen species formation as did N-acetyl-L-cysteine. More importantly, Pachymic acid inhibited nuclear factor-κB translocation.
CONCLUSIONS:
The property of Pachymic acid can mitigate the unfavorable conditions induced by AH Plus stimuli. Therefore, the use of Pachymic acid is suggested to prevent the complications of oral diseases such as inflammation and alveolar destruction of the oral cavity.

Pachymic acid stimulates glucose uptake through enhanced GLUT4 expression and translocation.[Pubmed: 20816811 ]

Eur J Pharmacol. 2010 Dec 1;648(1-3):39-49.

In an effort to investigate the effect and mechanism of Poria cocos on glucose uptake, six lanostane-type triterpenoids were isolated and analyzed.
METHODS AND RESULTS:
Among them, Pachymic acid displayed the most significant stimulating activity on glucose uptake in 3T3-L1 adipocytes. The effect of Pachymic acid on the expression profile of glucose transporters in differentiated 3T3-L1 adipocytes was also analyzed. Our results demonstrated that Pachymic acid induced an increase in GLUT4, but not GLUT1, expression at both the mRNA and protein levels. The role of GLUT4 was further confirmed using the lentiviral vector-derived GLUT4 short hairpin RNA (shRNA). The stimulating activity of Pachymic acid on glucose uptake was abolished when the endogenous GLUT4 expression was suppressed in 3T3-L1 adipocytes. In addition to increased GLUT4 expression, Pachymic acid stimulated GLUT4 redistribution from intracellular vesicles to the plasma membrane in adipocytes. Exposure of the differentiated adipocytes to Pachymic acid increased the phosphorylation of insulin receptor substrate (IRS)-1, AKT and AMP-activated kinase (AMPK). The involvement of PI3K and AMPK in the action of Pachymic acid was further confirmed as PI3K and AMPK inhibitors completely blocked the Pachymic acid-mediated activities in adipocytes. In addition, Pachymic acid was shown to induce triglyceride accumulation and inhibit lipolysis in differentiated adipocytes.
CONCLUSIONS:
Taken together, we demonstrated the insulin-like activities of this compound in stimulating glucose uptake, GLUT4 gene expression and translocation, and promoting triglyceride accumulation in adipocytes. Our study provides important insights into the underlying mechanism of hypoglycemic activity of P. cocos.

In vivo

Pachymic Acid Enhances Pentobarbital-Induced Sleeping Behaviors via GABAA-ergic Systems in Mice[Pubmed: 25143810]

Biomol Ther (Seoul). 2014 Jul; 22(4): 314–20.

This study was investigated to know whether Pachymic acid (PA), one of the predominant triterpenoids in Poria cocos (Hoelen) has the sedative-hypnotic effects, and underlying mechanisms are mediated via γ-aminobutyric acid (GABA)-ergic systems.
METHODS AND RESULTS:
Oral administration of PA markedly suppressed locomotion activity in mice. This compound also prolonged sleeping time, and reduced sleep latency showing synergic effects with muscimol (0.2 mg/kg) in shortening sleep onset and enhancing sleep time induced by pentobarbital, both at the hypnotic (40 mg/kg) and sub-hypnotic (28 mg/kg) doses. Additionally, PA elevated intracellular chloride levels in hypothalamic primary cultured neuronal cells of rats. Moreover, Western blotting quantitative results showed that PA increased the amount of protein level expression of GAD65/67 over a broader range of doses. PA increased α- and β-subunits protein levels, but decreased γ-subunit protein levels in GABAA receptors. The present experiment provides evidence for the hypnotic effects as PA enhanced pentobarbital-induced sleeping behaviors via GABAA-ergic mechanisms in rodents.
CONCLUSIONS:
Taken together, it is proposed that PA may be useful for the treatment of sleep disturbed subjects with insomnia.

Protocol of Pachymic acid

Cell Research

Pachymic acid protects H9c2 cardiomyocytes from lipopolysaccharide-induced inflammation and apoptosis by inhibiting the extracellular signal-regulated kinase 1/2 and p38 pathways.[Pubmed: 25936656]

Inhibition of ovarian cancer proliferation and invasion by pachymic acid.[Pubmed: 25973134]

Int J Clin Exp Pathol. 2015 Feb 1;8(2):2235-41. eCollection 2015.

To determine the effect of Pachymic acid (PA) on proliferation, cell cycle, and invasion in human ovarian carcinoma cell lines HO-8910 and explore some possible mechanisms, HO-8910 cells was treated with different concentrations of PA (0.5, 1, 2 μM).
METHODS AND RESULTS:
CCK-8 assay, propidium iodide staining, was applied to measuring the growth inhibiting rates of HO-8910 cells. Cell cycle was measured by flow cytometry. In addition, the activity of PA against HO-8910 cells invasion was evaluated in transwell assay. Western blot detected the proteins expression of E-cadherin, β-catenin and COX-2 of different groups treated with PA in different concentrations (0.5, 1, 2 μM) for 48 h. Our results showed that PA could effectively inhibit the in vitro growth of HO-8910 cells in dose-dependent manners in 72 h, suppressed migration and invasion of HO-8910 cells in concentration-dependent manners at 24 h, caused the increased accumulation of G1 phase cells, and caused down-regulation of β-catenin and COX-2 and up-regulation of E-cadherin expression level.
CONCLUSIONS:
Taken together, it could conclude that PA might inhibit proliferation and invasion of ovarian carcinoma cell through decreasing β-catenin and COX-2 expression and increasing E-cadherin expression.

Mol Med Rep. 2015 Apr 30. doi: 10.3892/mmr.2015.3712.

Pachymic acid (PA), a lanostane-type triterpenoid and the major component of Poria cocos alcoholic extracts, has various pharmacological effects, including anti-inflammatory, anti-oxidative and anti-apoptotic. However, few studies have investigated the effects of PA on lipopolysaccharide (LPS)-induced H9c2 cell apoptosis and inflammation, or identified the possible mechanisms underlying these effects.
CONCLUSIONS:
In the present study, H9c2 cardiomyocytes were stimulated by LPS and treated with or without PA. The increased mRNA expression levels of tumor necrosis factor-α, interleukin (IL)-1 and IL-6 induced by LPS were attenuated following treatment with PA. PA also attenuated LPS-induced apoptosis, as determined by a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and regulated the LPS-induced protein expression levels of caspase 3, 8 and 9. Furthermore, the phosphorylations of extracellular-regulated kinase (Erk)1/2 and p38 in the LPS-treated H9c2 cells were inhibited by PA.
CONCLUSIONS:
These results suggested that treatment with PA prevented the LPS-induced inflammatory and apoptotic response in cardiomyocytes, which may be mediated by inhibition of the Erk1/2 and p38 pathways.

Pachymic acid Dilution Calculator

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Preparing Stock Solutions of Pachymic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.8912 mL 9.4561 mL 18.9122 mL 37.8243 mL 47.2804 mL
5 mM 0.3782 mL 1.8912 mL 3.7824 mL 7.5649 mL 9.4561 mL
10 mM 0.1891 mL 0.9456 mL 1.8912 mL 3.7824 mL 4.728 mL
50 mM 0.0378 mL 0.1891 mL 0.3782 mL 0.7565 mL 0.9456 mL
100 mM 0.0189 mL 0.0946 mL 0.1891 mL 0.3782 mL 0.4728 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Pachymic acid

Pachymic acid is a lanostrane-type triterpenoid from P. cocos. Pachymic acid inhibits Akt and ERK signaling pathways.

In Vitro:Pachymic acid (PA) is able to inhibit gallbladder cancer tumorigenesis involving affection of Akt and ERK signaling pathways. Pachymic acid (PA) treatment significantly inhibits Rho A, Akt and ERK pathway in gallbladder carcinoma cells. Pachymic acid (PA) treatment can dose-dependently downregulate PCNA, ICAM-1, RhoA, p-Akt and pERK. Cell growth is inhibited by 10 µg/mL Pachymic acid (PA) 12 h after treatment, and a concentration of 30 µg/mL further reduced cell growth. The growth of cells is suppressed in a time- and dose-dependent manner. After 48 h treatment, about 25%, 40% and 70% of the cell growth are inhibited by Pachymic acid (PA) at concentration of 10 µg/mL, 20 µg/mL and 30 µg/mL, respectively. Pachymic acid (PA) also inhibits the growth of gallbladder carcinoma cells in a time-dependent and dose-dependent manner[1].

In Vivo:To evaluate the anti-tumor activity of Pachymic acid (PA) in vivo, human lung cancer NCI-H23 tumor xenograft models are used. Pachymic acid (PA) significantly suppresses tumor growth at doses of 30 and 60 mg/kg for 21 days compared with the control group[2].

References:
[1]. Chen Y, et al. Pachymic acid inhibits tumorigenesis in gallbladder carcinoma cells. Int J Clin Exp Med. 2015 Oct 15;8(10):17781-8. [2]. Ma J, et al. Pachymic acid induces apoptosis via activating ROS-dependent JNK and ER stress pathways in lung cancer cells. Cancer Cell Int. 2015 Aug 5;15:78.

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References on Pachymic acid

Inhibition of ovarian cancer proliferation and invasion by pachymic acid.[Pubmed:25973134]

Int J Clin Exp Pathol. 2015 Feb 1;8(2):2235-41. eCollection 2015.

To determine the effect of Pachymic acid (PA) on proliferation, cell cycle, and invasion in human ovarian carcinoma cell lines HO-8910 and explore some possible mechanisms, HO-8910 cells was treated with different concentrations of PA (0.5, 1, 2 muM). CCK-8 assay, propidium iodide staining, was applied to measuring the growth inhibiting rates of HO-8910 cells. Cell cycle was measured by flow cytometry. In addition, the activity of PA against HO-8910 cells invasion was evaluated in transwell assay. Western blot detected the proteins expression of E-cadherin, beta-catenin and COX-2 of different groups treated with PA in different concentrations (0.5, 1, 2 muM) for 48 h. Our results showed that PA could effectively inhibit the in vitro growth of HO-8910 cells in dose-dependent manners in 72 h, suppressed migration and invasion of HO-8910 cells in concentration-dependent manners at 24 h, caused the increased accumulation of G1 phase cells, and caused down-regulation of beta-catenin and COX-2 and up-regulation of E-cadherin expression level. Taken together, it could conclude that PA might inhibit proliferation and invasion of ovarian carcinoma cell through decreasing beta-catenin and COX-2 expression and increasing E-cadherin expression.

The antioxidant property of pachymic acid improves bone disturbance against AH plus-induced inflammation in MC-3T3 E1 cells.[Pubmed:23522537]

J Endod. 2013 Apr;39(4):461-6.

INTRODUCTION: The cytotoxicity of resin-based sealer is influential on the inflammatory reaction and cell survival for oral periapical cells. In this study, Pachymic acid as an antioxidant was investigated for the improvement of bone disturbance against AH Plus (Dentsply DeTrey GmbH, Konstanz, Germany)-induced inflammation in MC-3T3 E1 cells. METHODS: AH Plus was prepared according to the manufacturer's instructions. Using mouse osteoblast cells (MC-3T3 E1), a specimen of AH Plus was eluted with the culture medium for 1 day and was diluted by 30%. The cellular cytotoxicity and reactive oxygen species formation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and 2',7'-dichlorodihydrofluorescein diacetate with fluorescence-activated cell sorting. The secretion of proinflammatory cytokines was determined by an enzyme-linked immunosorbent assay, and the expression of inflammatory and osteogenic molecules was determined by immunoblotting. RESULTS: Cells with AH Plus elutes showed a decrease of cell viability and ALP activity. However, Pachymic acid and N-acetyl-L-cysteine (control antioxidant) restored cell viability and ALP activity damaged by AH plus. The secretion of nitric oxide, tumor necrosis factor alpha, and interleukin-1beta were increased in AH Plus-stimulated MC-3T3 E1 cells, but Pachymic acid suppressed its production. Furthermore, Pachymic acid reduced the receptor activator of nuclear factor-kappaB ligand, cyclooxygenase-2, matrix metalloproteinase-2 and -9, increased bone morphogenetic protein-2 and -7, and runt-related transcription factor 2 despite AH Plus stimuli. In addition, Pachymic acid affected the removal effect of reactive oxygen species formation as did N-acetyl-L-cysteine. More importantly, Pachymic acid inhibited nuclear factor-kappaB translocation. CONCLUSIONS: The property of Pachymic acid can mitigate the unfavorable conditions induced by AH Plus stimuli. Therefore, the use of Pachymic acid is suggested to prevent the complications of oral diseases such as inflammation and alveolar destruction of the oral cavity.

Pachymic acid stimulates glucose uptake through enhanced GLUT4 expression and translocation.[Pubmed:20816811]

Eur J Pharmacol. 2010 Dec 1;648(1-3):39-49.

In an effort to investigate the effect and mechanism of Poria cocos on glucose uptake, six lanostane-type triterpenoids were isolated and analyzed. Among them, Pachymic acid displayed the most significant stimulating activity on glucose uptake in 3T3-L1 adipocytes. The effect of Pachymic acid on the expression profile of glucose transporters in differentiated 3T3-L1 adipocytes was also analyzed. Our results demonstrated that Pachymic acid induced an increase in GLUT4, but not GLUT1, expression at both the mRNA and protein levels. The role of GLUT4 was further confirmed using the lentiviral vector-derived GLUT4 short hairpin RNA (shRNA). The stimulating activity of Pachymic acid on glucose uptake was abolished when the endogenous GLUT4 expression was suppressed in 3T3-L1 adipocytes. In addition to increased GLUT4 expression, Pachymic acid stimulated GLUT4 redistribution from intracellular vesicles to the plasma membrane in adipocytes. Exposure of the differentiated adipocytes to Pachymic acid increased the phosphorylation of insulin receptor substrate (IRS)-1, AKT and AMP-activated kinase (AMPK). The involvement of PI3K and AMPK in the action of Pachymic acid was further confirmed as PI3K and AMPK inhibitors completely blocked the Pachymic acid-mediated activities in adipocytes. In addition, Pachymic acid was shown to induce triglyceride accumulation and inhibit lipolysis in differentiated adipocytes. Taken together, we demonstrated the insulin-like activities of this compound in stimulating glucose uptake, GLUT4 gene expression and translocation, and promoting triglyceride accumulation in adipocytes. Our study provides important insights into the underlying mechanism of hypoglycemic activity of P. cocos.

Anti-inflammatory effect of pachymic acid promotes odontoblastic differentiation via HO-1 in dental pulp cells.[Pubmed:22849812]

Oral Dis. 2013 Mar;19(2):193-9.

OBJECTIVES: Heme oxygenase-1 (HO-1) is contributed to odontoblast differentiation in human dental pulp cells (HDPCs). In this study, Pachymic acid from mushroom Formitopsis niagra is examined to determine whether it affects pulpal inflammation and promotes odontogenesis via HO-1 gene expression. MATERIALS AND METHODS: The HDPCs were given H2O2 for inflammation. The anti-inflammatory character and odontoblast differentiation by Pachymic acid were analyzed by Western blotting, alkaline phosphatase activity, and alizarin red S staining. To understand the mechanism of Pachymic acid via HO-1 induction, the cells were treated with zinc protoporphyrin IX (ZnPP: HO-1 inhibitor). RESULTS: H2O2 induced pulp inflammation and disturbed odontoblast differentiation. However, the HDPCs treated with Pachymic acid affected anti-inflammatory effect and induction of odontoblast differentiation through increasing HO-1 expression. In addition, Pachymic acid has potent cytoprotection and mineralization under H2O2 treatment. Furthermore, Pachymic acid significantly suppressed nuclear factor-kappa B (NF-kappaB) translocation into nucleus and induced NE-E2-related factor-2 (Nrf2) translocation into nucleus. Overall, NF-kappaB and Nrf2 translocation were regulated by the HO-1 pathway. CONCLUSIONS: The Pachymic acid showed anti-inflammatory function and odontoblast differentiation via HO-1 pathway. These results suggested that Pachymic acid may be applicable for prevention of oral inflammation or to improve dentin mineralization against several stresses.

Pachymic Acid Enhances Pentobarbital-Induced Sleeping Behaviors via GABAA-ergic Systems in Mice.[Pubmed:25143810]

Biomol Ther (Seoul). 2014 Jul;22(4):314-20.

This study was investigated to know whether Pachymic acid (PA), one of the predominant triterpenoids in Poria cocos (Hoelen) has the sedative-hypnotic effects, and underlying mechanisms are mediated via gamma-aminobutyric acid (GABA)-ergic systems. Oral administration of PA markedly suppressed locomotion activity in mice. This compound also prolonged sleeping time, and reduced sleep latency showing synergic effects with muscimol (0.2 mg/kg) in shortening sleep onset and enhancing sleep time induced by pentobarbital, both at the hypnotic (40 mg/kg) and sub-hypnotic (28 mg/kg) doses. Additionally, PA elevated intracellular chloride levels in hypothalamic primary cultured neuronal cells of rats. Moreover, Western blotting quantitative results showed that PA increased the amount of protein level expression of GAD65/67 over a broader range of doses. PA increased alpha- and beta-subunits protein levels, but decreased gamma-subunit protein levels in GABAA receptors. The present experiment provides evidence for the hypnotic effects as PA enhanced pentobarbital-induced sleeping behaviors via GABAA-ergic mechanisms in rodents. Taken together, it is proposed that PA may be useful for the treatment of sleep disturbed subjects with insomnia.

Pachymic acid protects H9c2 cardiomyocytes from lipopolysaccharide-induced inflammation and apoptosis by inhibiting the extracellular signal-regulated kinase 1/2 and p38 pathways.[Pubmed:25936656]

Mol Med Rep. 2015 Aug;12(2):2807-13.

Pachymic acid (PA), a lanostane-type triterpenoid and the major component of Poria cocos alcoholic extracts, has various pharmacological effects, including anti-inflammatory, anti-oxidative and anti-apoptotic. However, few studies have investigated the effects of PA on lipopolysaccharide (LPS)-induced H9c2 cell apoptosis and inflammation, or identified the possible mechanisms underlying these effects. In the present study, H9c2 cardiomyocytes were stimulated by LPS and treated with or without PA. The increased mRNA expression levels of tumor necrosis factor-alpha, interleukin (IL)-1 and IL-6 induced by LPS were attenuated following treatment with PA. PA also attenuated LPS-induced apoptosis, as determined by a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and regulated the LPS-induced protein expression levels of caspase 3, 8 and 9. Furthermore, the phosphorylations of extracellular-regulated kinase (Erk)1/2 and p38 in the LPS-treated H9c2 cells were inhibited by PA. These results suggested that treatment with PA prevented the LPS-induced inflammatory and apoptotic response in cardiomyocytes, which may be mediated by inhibition of the Erk1/2 and p38 pathways.

Description

Pachymic acid is a lanostrane-type triterpenoid from P. cocos. Pachymic acid inhibits Akt and ERK signaling pathways.

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