Pseudolaric Acid B targets multiple pathways and proteins. It is a microtubule-destabilizing agent, meaning it interferes with the polymerization of tubulin into microtubules. This disrupts the mitotic spindle, leading to cell cycle arrest and apoptosis. It is a PPARalpha signaling agonist. It inhibits NF-kappaB and p38 signaling, contributing to its anti-inflammatory effects. By inhibiting angiogenesis, it blocks the formation of new blood vessels, which is important for tumor growth. Its ability to induce both apoptosis and autophagy contributes to its antitumor activity.

In vitro, Pseudolaric Acid B displays antifungal activity against a variety of fungi. It induces apoptosis in cancer cell lines. As a microtubule-destabilizing agent, it causes cell cycle arrest and cell death. It inhibits angiogenesis in vitro by suppressing endothelial cell proliferation and tube formation. It also exhibits anti-inflammatory activity by inhibiting NF-kappaB and p38 signaling. Its activity as a PPARalpha agonist has been confirmed in cell-based reporter assays. These diverse in vitro activities make it a compound of interest for studying cancer, inflammation, and angiogenesis.

In vivo, Pseudolaric Acid B has been shown to possess antifungal, antifertility, and antitumor activities. It has been reported to have antitumor effects in animal models. Its antifungal activity has been demonstrated in vivo against various fungal pathogens. Its antifertility properties have also been observed in animal studies. As an angiogenesis inhibitor, it has been shown to reduce tumor growth in vivo by blocking blood vessel formation. These in vivo studies confirm the multifunctional nature of Pseudolaric Acid B.

The in vitro assays for Pseudolaric Acid B measure its effects on various targets. To assess its microtubule-destabilizing activity, a tubulin polymerization assay is used. Purified tubulin is incubated with Pseudolaric Acid B, and the formation of microtubules is measured spectrophotometrically. The inhibition of polymerization is calculated. For its anti-inflammatory activity, its ability to inhibit NF-kappaB activation can be measured using a reporter gene assay in cells stimulated with TNF-α. Its antifungal activity is assessed using standard broth microdilution assays to determine the minimum inhibitory concentration (MIC) against various fungal strains.

In vitro cell-based assays for Pseudolaric Acid B are used to study its effects on cancer cells, endothelial cells, and immune cells. For anti-cancer studies, cancer cell lines are treated with Pseudolaric Acid B, and cell viability is assessed using MTT or CellTiter-Glo assays. Apoptosis is measured using Annexin V staining or caspase-3/7 activation assays. Autophagy is assessed by measuring the conversion of LC3-I to LC3-II or by detecting autophagosomes. For anti-angiogenic studies, endothelial cells are treated with the compound, and their ability to form capillary-like structures in a Matrigel tube formation assay is assessed. These cell-based assays confirm its multifunctional activity.

In vivo animal experiments for Pseudolaric Acid B are conducted in models of cancer, fungal infection, and fertility. In a typical antitumor study, mice bearing xenograft tumors are treated with Pseudolaric Acid B, and tumor growth is monitored. For antifungal studies, animals infected with a fungal pathogen are treated with the compound, and survival or fungal burden is assessed. For antifertility studies, the effects on reproductive function are evaluated in animal models. The compound is typically administered by injection. These studies provide evidence for its in vivo efficacy.

Pseudolaric Acid B has a molecular weight of 432.5 g/mol and a molecular formula of C23H28O8. It is a white to off-white solid with a purity of ≥98% (HPLC). It is soluble in DMSO, ethanol, methanol, and chloroform. For storage, it is recommended to keep the compound at 4°C. Detailed pharmacokinetic properties such as absorption, distribution, metabolism, and excretion (ADME) have not been extensively characterized. As a natural product, its bioavailability and half-life would need to be determined through specific studies.

Detailed toxicity data for Pseudolaric Acid B is not provided in standard product descriptions. However, as a compound with antifertility and antitumor properties, it is expected to have significant biological activity and potential toxicity. Its effects on the reproductive system indicate it can have endocrine or cellular effects. As with all research chemicals, standard laboratory safety precautions should be followed when handling Pseudolaric Acid B. Its use is limited to research applications and it is not intended for human or veterinary use.

[1]. Some progress on the chemistry of natural bioactive terpenoids from Chinese medicinal plants. Mem Inst Oswaldo Cruz. 1991;86 Suppl 2:219-26.

[2]. [Endocrine activity of pseudolaric acids A and B and their effects on sex hormones, prostaglandins, uteri, and fetuses]. Zhongguo Yao Li Xue Bao. 1991 Mar;12(2):187-90.

[3]. The immunosuppressive activity of pseudolaric acid B on T lymphocytes in vitro. Phytother Res. 2013 Jul;27(7):980-5.

[4]. Pseudolaric acid B inhibits the secretion of hepatitis B virus. Oncol Rep. 2017 Jan;37(1):519-525.

[5]. Pseudolaric acid B activates autophagy in MCF-7 human breast cancer cells to prevent cell death. Oncol Lett. 2016 Mar;11(3):1731-1737.

Therapeutic Uses
Traditional Chinese Medicine
Exploring Treatments Candida albicans is one of the most common fungal pathogens in humans. The emergence of resistance to azole antifungal drugs has raised the question of combination therapy to optimize treatment efficacy. This study aimed to evaluate the in vitro synergistic effect of pseudolarial acid B (PAB) and fluconazole (FLC) against clinically isolated Candida albicans. The in vitro antifungal activity of PAB (a diterpenic acid from P. albicans) alone and in combination with FLC against 22 FLC-resistant (FLC-R) and 12 FLC-sensitive (FLC-S) Candida albicans strains was evaluated using the checkerboard microdilution method and time-kill assay. Synergistic effects were observed in all 22 (100%) FLC-R strains, determined by the partial inhibition concentration index (FICI) (range 0.02 to 0.13) and the Bliss independence (BI) model. Of the 12 FLC-S strains, 2 (17%) showed synergistic effects using the FICI model (values ranging from 0.25 to 0.5), while 3 (18%) showed synergistic effects using the BI model. For the FLC-R strains, the synergistic FLC and PAB concentrations ranged from 0.06 to 4 μg mL⁻¹ and 0.5 to 4 μg mL⁻¹, respectively. For the FLC-S strains, the concentrations ranged from 1 to 8 μg mL⁻¹ and 0.5 to 4 μg mL⁻¹, respectively. The results of the BI model were consistent with those of the FICI model, but no antagonistic activity was observed in any of the tested strains. The interaction between PAB and FLC was confirmed using time-kill assays against the selected strains. Fluconazole and PAB showed good synergistic effects against azole-resistant Candida albicans isolates.
Exploring treatments for candidiasis is an opportunistic infection common in HIV-infected individuals. Approximately 90% of patients with HIV/AIDS develop oral and/oropharyngeal candidiasis at different stages. Triazole antifungals, such as fluconazole and itraconazole, are considered the first-line drugs for the treatment and prevention of candidiasis due to their relatively low side effects and high efficacy against mucosal infections. However, long-term exposure to azole drugs can lead to drug resistance, which poses a challenge for both clinicians and patients. In Traditional Chinese Medicine (TCM), over 300 herbs have been identified as having "bactericidal" properties, some of which have been used clinically as antifungal drugs for many years. Crude extracts of many TCM herbs have shown antifungal activity in in vitro experiments, including peony bark, larch bark, galangal, coptis, clove, cinnamon, anemarrhena, phellodendron bark, cassia twig, and gallnut. Identified effective anti-Candida components include berberine, palmatine, allicin, larchic acid A and B, magnolol, and magnolol and galangin. Therefore, TCM provides a rich selection for treating refractory candidiasis, a common ailment in HIV/AIDS patients. However, further screening of the effective extracts and investigation of their antifungal mechanisms are still needed. Importantly, the safety of these compounds must be fully demonstrated before clinical application.

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Pseudolaric Acid B is a research compound and is not approved for any clinical or therapeutic use. It is a natural diterpenoid isolated from Pseudolarix kaempferi with a broad spectrum of biological activities, including antifungal, antifertility, antitumor, anti-inflammatory, and anti-angiogenic effects. It acts as a microtubule-destabilizing agent, a PPARalpha agonist, and an inhibitor of NF-kappaB and p38 signaling. It induces apoptosis and autophagy. Pseudolaric Acid B is a valuable research tool for studying cancer biology, angiogenesis, inflammation, and fungal infections. However, it is not a drug and has not undergone clinical trials.

C23H28O8

432.46

432.178

82508-31-4

6475943

White to off-white solid powder

1.3±0.1 g/cm3

613.8±55.0 °C at 760 mmHg

166°C

208.8±25.0 °C

0.0±3.8 mmHg at 25°C

1.565

2.78

1

8

7

31

913

4

C/C(=C\C=C\[C@@]1([C@@H]2CC[C@@]3([C@@]2(CCC(=CC3)C(=O)OC)OC(=O)C)C(=O)O1)C)/C(=O)O

VDGOFNMYZYBUDT-YDRCMHEVSA-N

InChI=1S/C23H28O8/c1-14(18(25)26)6-5-10-21(3)17-9-12-22(20(28)31-21)11-7-16(19(27)29-4)8-13-23(17,22)30-15(2)24/h5-7,10,17H,8-9,11-13H2,1-4H3,(H,25,26)/b10-5+,14-6+/t17-,21+,22+,23-/m0/s1

(2E,4E)-5-[(1R,7S,8S,9R)-7-acetyloxy-4-methoxycarbonyl-9-methyl-11-oxo-10-oxatricyclo[6.3.2.01,7]tridec-3-en-9-yl]-2-methylpenta-2,4-dienoic acid

Pseudolaric Acid B (-)-Pseudolaric acid B Pseudolaric Acid-B

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

DMSO : ~50 mg/mL (~115.62 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (5.78 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (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 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL 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: ≥ 2.08 mg/mL (4.81 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 20.8 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: ≥ 2.08 mg/mL (4.81 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 20.8 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.)