The study does not identify a direct molecular target. Pachymic acid inhibits the phosphorylation of AKT and ERK1/2 signaling pathways. It also downregulates the expression of oncoproteins including PCNA, ICAM-1, and RhoA. [1]

Pachymic Acid (PA) has the ability to affect gallbladder carcinogenesis by blocking Akt and ERK signaling. Treatment with pachymic acid (PA) greatly reduced the gallbladder's Rho A, Akt, and ERK balance. Treatment with pazamic acid (PA) degrades PCNA, ICAM-1, RhoA, p-Akt, and pERK in a dose-dependent manner. Ten micrograms per milliliter of Pachymic Acid (PA) decreased cell growth twelve hours after treatment, and thirty micrograms per milliliter further suppressed cell development. Time was used to measure the rate of cell growth, and after 48 hours of treatment, poria acid (PA) at doses of 10 μg/mL, 20 μg/mL, and 30 μg/mL inhibited roughly 25%, 40%, and 70% of cell growth, respectively. Gallbladder dye development is still inhibited by pachymic acid (PA) in a dose- and time-dependent manner [1].

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Pachymic acid significantly reduces the growth of human gallbladder carcinoma GBC-SD cells in a dose- and time-dependent manner. After 48 hours of treatment, cell growth was inhibited by approximately 25%, 40%, and 70% at concentrations of 10, 20, and 30 μg/ml, respectively, as measured by CCK-8 assay. [1]
Pachymic acid induces cell cycle arrest at the G0/G1 phase in a dose-dependent manner. Flow cytometry analysis showed a significant increase in the percentage of cells in G1 phase and a corresponding decrease in S phase after treatment with 20 and 30 μg/ml PA for 24 hours. The G2/M phase population was not significantly affected. [1]
Pachymic acid significantly inhibits the migration of GBC-SD cells in a dose-dependent manner, as determined by Transwell migration assay after 16 hours of treatment with 10, 20, and 30 μg/ml PA. [1]
Pachymic acid significantly inhibits the invasion of GBC-SD cells in a dose-dependent manner, as determined by Matrigel invasion assay after treatment with 10, 20, and 30 μg/ml PA. [1]
Pachymic acid inhibits the adhesion of GBC-SD cells to fibronectin-coated plates. Treatment with 20 μg/ml and 30 μg/ml PA for 60 minutes significantly reduced cell adhesion, while 10 μg/ml showed a trend toward reduction (p=0.059). [1]
Western blot analysis showed that pachymic acid treatment (10, 20, 30 μg/ml for 24 hours) dose-dependently downregulated the expression of PCNA, ICAM-1, and RhoA proteins in GBC-SD cells. [1]
Pachymic acid dose-dependently inhibited the phosphorylation of AKT and ERK1/2 without affecting their total protein levels in GBC-SD cells, as shown by Western blot. [1]

Pachymic Acid (PA) anticancer activity was assessed in vivo using the NCI-H23 tumor xenograft model for human lung cancer. At doses of 30 and 60 mg/kg, Pachymic Acid (PA) effectively suppressed tumor growth for 21 days when compared with the coordinate system [2].

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In an NCI-H23 xenograft mouse model, pachymic acid significantly suppressed tumor growth at doses of 30 and 60 mg/kg administered via intraperitoneal injection for 21 days (5 days/week) compared to vehicle control. [2]
Immunohistochemical analysis of tumor xenografts showed that pachymic acid decreased the expression of proliferation marker Ki-67 and increased the number of TUNEL-positive apoptotic cells. [2]
Immunohistochemical analysis also showed that pachymic acid increased p-JNK and CHOP expression in tumor xenograft tissues, consistent with in vitro findings. [2]
No significant body weight loss was observed in PA-treated mice compared to vehicle control, indicating tolerability. [2]

Cell Culture: Human gallbladder carcinoma GBC-SD cells were cultured in DMEM medium supplemented with 10% fetal bovine serum, 10 mM HEPES, and antibiotics (100 U/mL penicillin and 100 mg/mL streptomycin) at 37°C in a 5% CO₂ humidified incubator. Pachymic acid was dissolved in DMSO at a stock concentration of 20 mM and diluted to working concentrations (10, 20, 30 μg/ml). Control treatments contained an equivalent concentration of DMSO (0.1%). [1]
Cell Viability Assay (CCK-8): Cells were treated with indicated concentrations of pachymic acid for 12, 24, and 48 hours. After treatment, 10 μl of CCK-8 solution was added to each well and incubated for 1 hour. Absorbance was measured at 450 nm using a microplate reader. [1]
Cell Cycle Analysis: After treatment with pachymic acid for 24 hours, cells were harvested, fixed in 80% cold ethanol at 4°C for 15 minutes, and centrifuged. Cell pellets were resuspended in propidium iodide (10 μg/ml) containing RNase (300 μg/ml) and incubated on ice for 30 minutes. Cells were filtered through 53 μm nylon mesh, and cell cycle distribution was analyzed by flow cytometry using ModFit LT software. [1]
Migration and Invasion Assays: For migration assay, cells (1 × 10⁵) in serum-free DMEM with 1% FBS were added to the upper chamber of Transwell inserts. The lower chamber contained DMEM with 10% FBS as a chemoattractant. After 16 hours of incubation, cells on the upper surface were removed, and cells on the lower surface were stained with crystal violet and counted under a light microscope. For invasion assay, Matrigel-coated Transwell chambers were used following the same procedure. [1]
Cell Adhesion Assay: 12-well plates were coated with fibronectin overnight at 4°C. Wells were rinsed with PBS, blocked with 0.1% BSA in PBS for 1 hour, and preheated to 37°C. Cells (1 × 10⁵ per well) were plated and incubated for 60 minutes with or without pachymic acid. After incubation, cells were treated with percoll flotation medium and fixative, washed with PBS, stained with 0.5% crystal violet, and counted. [1]
Western Blot Analysis: After treatment with pachymic acid for 24 hours, cells were lysed with RIPA buffer. Protein samples (30 μg) were subjected to SDS-PAGE, transferred to PVDF membranes, and blocked. Membranes were incubated with primary antibodies against total AKT (1:1000), pAKT (1:1000), total ERK1/2 (1:1000), pERK1/2 (1:1000), GAPDH (1:1500), PCNA (1:10000), ICAM-1 (1:200), and RhoA (1:1000) overnight at 4°C, followed by secondary antibody incubation. Proteins were visualized using ECL Plus reagent and exposed to X-ray film. [1]

Pachymic acid is a lanostane-type triterpenoid isolated from the sclerotium of *Poria cocos* (also called Fuling in traditional Chinese medicine) and from the European fungus *Fomitopsis pinicola*. [1]
* It has been reported to possess anti-emetic, anti-inflammatory, and anti-cancer properties. Previous studies have shown that pachymic acid inhibits tumor formation in mouse skin, activates Epstein-Barr virus early antigen in Raji cells, and suppresses growth, invasion, or metastasis in lung, breast, and pancreatic cancer cells. [1]
* This is the first study to investigate the effects of pachymic acid on gallbladder carcinoma cells. The results demonstrate that pachymic acid inhibits tumorigenesis in gallbladder cancer cells by suppressing cell growth (via G1 phase arrest), migration, invasion, and adhesion. [1]
* The anti-tumor effects of pachymic acid are mediated, at least in part, through inhibition of AKT and ERK signaling pathways and downregulation of oncoproteins PCNA, ICAM-1, and RhoA. [1]
* The study suggests that pachymic acid may be a promising candidate for gallbladder cancer therapy. [1]

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Pachymic acid is a lanostane-type triterpenoid isolated from the sclerotium of Poria cocos (also called Fuling in traditional Chinese medicine) and from the European fungus Fomitopsis pinicola. [1]
It has been reported to possess anti-emetic, anti-inflammatory, and anti-cancer properties. Previous studies have shown that pachymic acid inhibits tumor formation in mouse skin, activates Epstein-Barr virus early antigen in Raji cells, and suppresses growth, invasion, or metastasis in lung, breast, and pancreatic cancer cells. [1]
This is the first study to investigate the effects of pachymic acid on gallbladder carcinoma cells. The results demonstrate that pachymic acid inhibits tumorigenesis in gallbladder cancer cells by suppressing cell growth (via G1 phase arrest), migration, invasion, and adhesion. [1]
The anti-tumor effects of pachymic acid are mediated, at least in part, through inhibition of AKT and ERK signaling pathways and downregulation of oncoproteins PCNA, ICAM-1, and RhoA. [1]
The study suggests that pachymic acid may be a promising candidate for gallbladder cancer therapy. [1]

No significant body weight loss was observed in PA-treated mice compared to vehicle control, indicating tolerability at the tested doses. [2]
H&E staining of lungs, liver, kidney, and spleen from PA-treated mice showed no significant differences in histological findings compared to control group, indicating no apparent organ toxicity at the tested doses. [2]

[1]. Pachymic acid inhibits tumorigenesis in gallbladder carcinoma cells. Int J Clin Exp Med. 2015 Oct 15;8(10):17781-8.

[2]. 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.

Pachymic acid is a triterpenoid compound. It has been reported to exist in Rhodofomitopsis lilacinogilva, Fomitopsis pinicola, and other organisms with relevant data. See also: Smilax china root (partial).

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Pachymic acid is a lanostane-type triterpenoid isolated from Poria cocos (Fuling), which is an important component in traditional Chinese medicine for treating breast cancer metastasis. [2]
Previous studies have shown that pachymic acid possesses anti-emetic, anti-inflammatory, and anti-cancer properties, including induction of apoptosis in prostate cancer cells. [2]
This study demonstrates for the first time that pachymic acid induces G2/M phase arrest and apoptosis in lung cancer cells through ROS-dependent activation of JNK and ER stress pathways. [2]
The anti-tumor effects were confirmed in an NCI-H23 xenograft model, where pachymic acid inhibited tumor growth without causing host toxicity, and these effects were associated with increased p-JNK and CHOP expression in tumor tissues. [2]
The study suggests that pachymic acid could be a promising agent for lung cancer therapy. [2]

528.381

29070-92-6

29070-92-6 CCRIS 7792

5484385

White to off-white solid powder

1.1±0.1 g/cm3

612.2±55.0 °C at 760 mmHg

184.7±25.0 °C

0.0±4.0 mmHg at 25°C

1.540

8.59

2

5

8

38

1020

8

O([H])[C@]1([H])C([H])([H])[C@@]2(C([H])([H])[H])C3C([H])([H])C([H])([H])[C@@]4([H])C(C([H])([H])[H])(C([H])([H])[H])[C@]([H])(C([H])([H])C([H])([H])[C@]4(C([H])([H])[H])C=3C([H])([H])C([H])([H])[C@]2(C([H])([H])[H])[C@@]1([H])[C@]([H])(C(=O)O[H])C([H])([H])C([H])([H])C(=C([H])[H])C([H])(C([H])([H])[H])C([H])([H])[H])OC(C([H])([H])[H])=O

VDYCLYGKCGVBHN-DRCQUEPLSA-N

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)/t22-,25-,26+,27+,28+,31-,32-,33+/m1/s1

(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

Pachymic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~10 mg/mL (~18.91 mM)
Ethanol : ~4.17 mg/mL (~7.89 mM)
H2O : < 0.1 mg/mL

Solubility in Formulation 1: 1 mg/mL (1.89 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 10.0 mg/mL clear DMSO stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: 1 mg/mL (1.89 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 10.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 1 mg/mL (1.89 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 10.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)