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Pachymic acid

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-P1001

  • Specification : 98%

  • CAS number : 29070-92-6

  • Formula : C33H52O5

  • Molecular Weight : 528.76

  • PUBCHEM ID : 5484385

  • Volume : 5mg

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Catalogue Number

BF-P1001

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

528.76

Appearance

White flake crystals

Botanical Source

Poria cocos

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

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

Synonyms

pachimic acid/Lanost-8-en-21-oic acid, 3-(acetyloxy)-16-hydroxy-24-methylene-, (3β,16α)-/3-O-Acetyltumulosic acid/3-ACETYLTUMULOSIC ACID/Lanost-8-en-21-oic acid,3-(acetyloxy)-16-hydroxy-24-methylene-,(3beta,16alpha)/(3β,16α)-3-Acetoxy-16-hydroxy-24-methylenelanost-8-en-21-oic acid/Pachymasaeure/(3b,16a)-3-(Acetyloxy)-16-hydroxy-24-methylenelanost-8-en-21-oic acid/Lanost-8-en-21-oic acid,3-(acetyloxy)-16-hydroxy/pachymaic acid

IUPAC Name

(2R)-2-[(3S,5R,10S,13R,14R,16R,17R)-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

Density

1.1±0.1 g/cm3

Solubility

Methanol; Chloroform

Flash Point

184.7±25.0 °C

Boiling Point

612.2±55.0 °C at 760 mmHg

Melting Point

InChl

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)

InChl Key

VDYCLYGKCGVBHN-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:29070-92-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29157832

Abstract

Background: The insulin-like growth factor 1 (IGF-1) signaling pathway has spotlighted as a mechanism to elucidate aging associated with autophagy in recent years. Therefore, we have tried to screen an effective compound capable of inducing autophagy to delay aging process.
Purpose: The aim of this study is to investigate whether pachymic acid, a main compound in Poria cocos, induces autophagy in the aged cells.
Methods: The aging of young cells was induced by treatment with IGF-1 at 50 ng/ml three times every two days. The effect of pachymic acid on cell viability was evaluated in human lung fibroblasts, WI-38 cells, using MTT assay. The induction of autophagy was detected using autophagy detection kit. The expression of proteins related to autophagy and IGF-1 signaling pathway was examined by western blot analysis and immunofluorescence assay.
Results: In this study, pachymic acid showed cytotoxic effect in a dose dependent manner and remarkably induced autophagy at the same time. Moreover, pachymic acid increased the expression of proteins related to autophagy such as LC3-II and Beclin1 and decreased the levels of mTor phosphorylation and p70S6K in the aged cells. In particular, pachymic acid increased the expression of p-PI3K, p-FoxO and Catalase. In addition, pachymic acid remarkably increased the expression of IGFBP-3.
Conclusion: Above results suggest that pachymic acid could induce autophagy related to IGF-1 signaling pathway in the aged cells.

KEYWORDS

Autophagy; FoxO; IGF-1; IGFBP-3; Pachymic acid; Poria cocos.

Title

Pachymic Acid Promotes Induction of Autophagy Related to IGF-1 Signaling Pathway in WI-38 Cells

Author

Su-Gyeong Lee 1 , Moon-Moo Kim 2

Publish date

2017 Dec 1

PMID

27792037

Abstract

Pachymic acid (PA), a lanostane-type triterpenoid derived from traditional Chinese herbals, has been reported to have antitumor activity in versatile cancer cells. However, the antitumor effect of PA in gastric cancer (GC) cells remains unclear. In this study, we aimed to explore the efficacy and mechanisms of PA in GC. The antiproliferative effect of PA was assessed by a growth assay and a colony formation assay. Flow cytometry was used to detect changes in cell cycle distribution. Apoptosis was assessed by an annexin V/propidium iodide double-staining assay. The expressions of the apoptosis-related proteins were measured by western blot. The mitochondrial capacity was observed by immunostaining of Mito Tracker Red and mitochondrial function protein MT. Xenograft models of GC were constructed by a subcutaneous injection of SGC-7901 and MKN-49P cells pretreated with PA. PA could potently inhibit GC cell growth and colony formation. PA significantly induced G1, G2/M, and inhibited G0 phase arrest in GC cell lines SGC-7901 and MKN-49P. PA induced cell apoptosis by regulating the expressions of apoptosis-related proteins (caspase-3, PARP, Bcl-2, and Bax) and suppressing the mitochondrial capacity of GC cell lines in vitro in a dose-dependent manner. In addition, PA suppressed the tumor growth of xenograft models of GC and prolonged the survival of animals markedly. In brief, the present study shows that PA induces apoptosis through inhibition of mitochondrial capacity in human GC cells. Our findings suggest that PA may have therapeutic potential in GC.

KEYWORDS

Autophagy; FoxO; IGF-1; IGFBP-3; Pachymic acid; Poria cocos.

Title

Pachymic Acid Inhibits the Tumorigenicity of Gastric Cancer Cells by the Mitochondrial Pathway

Author

Chunwei Lu 1 , Jun Ma, Dingfang Cai

Publish date

2017 Feb

PMID

30013646

Abstract

The aim of the present study was to elucidate the anticancer effect of pachymic acid (PA) in gastric cancer SGC-7901 cells and the potential molecular mechanisms involved. Cell Count kit-8 assay was performed to examine the effect of PA on the cell proliferation of SGC-7901 cells. Cell cycle, cell apoptosis, mitochondria membrane potential (Dψm) and reactive oxygen species (ROS) analysis were assessed by flow cytometry, respectively. DNA fragmentation assay was performed by Hoechst 33258 staining. Western blotting was performed to detect the effect of various concentrations of PA on the levels of BCL2 associated X protein (Bax) expression as well as B-cell lymphoma 2 (Bcl-2), cytochrome C (cyt-c) and caspase-3 in SGC-7901 cells. It was demonstrated that PA was able to significantly inhibit the viability and induce G0/G1 cell cycle arrest of SGC-7901 cells in a concentration-dependent manner. The apoptotic rate and ROS generation were markedly increased, while Dψm was decreased following the treatment of SGC-7901 cells with various concentrations of PA. Moreover, the expression of Bax, cytochrome c and caspase-3 were markedly increased and Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) was significantly inactivated and BCL-2 expression was decreased following PA treatment in SGC-7901 cells. Notably, JAK2 inhibitor (AG490) mimics the effects of PA on the viability and apoptosis of SGC-7901 cells. Further in vivo study indicated that treatment with PA significantly inhibited the growth of tumor in nude mice that were transplanted with SGC-7901 cells in a concentration-dependent manner. These results may advance the current understanding of the anticancer mechanisms of PA in gastric cancer.

KEYWORDS

Janus kinase 2/signal transducer and activator of transcription 3; apoptosis; gastric cancer; mitochondrial pathway; pachymic acid.

Title

Pachymic Acid Inhibits Growth and Induces Cell Cycle Arrest and Apoptosis in Gastric Cancer SGC-7901 Cells

Author

Kuan-Xue Sun 1 2 , Hong-Wei Xia 2

Publish date

2018 Aug


Description :

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