International Journal of Drug Delivery Technology
Volume 16, Issue 4s

Synthesis and Biological Evaluation of Piperic Acid and 4-Ethylpiperic Acid β-Amino Acid Conjugates as Anticancer Agents Targeting PI3K/Akt/NF-κB Signaling in Pancreatic Cancer Cells

Preeti Shrivastava1, Pranjal Upadhyay2, Maila Swapna3, B. Madhavilatha4, Yasmin Khatoon5, Mounica Peela6, Siddharth Sharma7, Sonu8*

1Faculty, Department of Biochemistry, Mata Jijabai Govt PG Girls College, Indore, Madhya Pradesh 452001 India
2Intern, Datta Meghe Medical College (DMIHER), Wanadongri, Hingna, Nagpur, 441110 India
3Assistant Professor, Nalla Narsimha Reddy Education Society's Group of Institutions- Integrated Campus, Medchal Malkajgiri, Telangana 500088 India
4Associate Professor, Nalla Narsimha Reddy Education Society's Group of Institutions- Integrated Campus, Medchal Malkajgiri, Telangana 500088 India
5Professor, Institute of Pharmacy, Shri Ramswaroop Memorial University, Barabanki, Lucknow, Uttar Pradesh 225003 India
6Assistant Professor, Vignan Institute of Pharmaceutical Technology (A), Duvvada, Kapujaggarajupeta, Visakhapatnam, Andhra Pradesh 530049 India
7Assistant Professor, Chandigarh Pharmacy College, CGC University, Mohali, Punjab 140307 India
8*Assistant Professor, School of Pharmaceutical Sciences, Rayat Bahra University, Village - Sahauran, Tehsil- Kharar, Mohali, Punjab, 140104 India

(Corresponding Author)

ABSTRACT

Background: Pancreatic cancer is one of the most aggressive malignancies with limited therapeutic options, primarily due to late detection, invasive behavior, and resistance to chemotherapy. The phosphatidylinositol 3-kinase (PI3K)/Akt/NF-κB signaling axis is constitutively activated in pancreatic tumors, driving proliferation, survival, and metastasis. Natural product scaffolds such as piperic acid (PA) and 4-ethylpiperic acid (EPA) have shown anticancer activity, and incorporation of β-amino acids has been proposed to enhance stability and potency.

Methods: In this study, PA and EPA were conjugated with β-amino acids via carbodiimide-mediated coupling. The resulting conjugates were structurally confirmed using FTIR, NMR, and mass spectrometry. Biological evaluation was performed against PC-3 (prostate), PANC-1 (pancreatic), and HCT-116 (colorectal) cell lines using cytotoxicity (MTT assay), clonogenic, wound-healing, Matrigel invasion, 3D collagen invasion, cell scattering, and fluorescent gelatin degradation assays. Apoptosis was assessed by DAPI staining, caspase-3/7 activity, and PARP cleavage. Western blotting was used to evaluate PI3K/Akt/NF-κB, MAPK/ERK, MMP-2/9, TIMP-1, and E-cadherin expression, while cell cycle effects were analyzed using FUCCI sensor technology.

Results: Among all derivatives, conjugates 5 (PA-based) and 20 (EPA-based) exhibited the most potent activity. Conjugate 5 induced apoptosis in PANC-1 cells (IC₅₀ ~7.0 μM) via PARP and caspase-3 cleavage, BAX upregulation, BCL2/XIAP downregulation, G2 arrest, and inhibition of MAPK/ERK phosphorylation. Conjugate 20 strongly inhibited migration, clonogenicity, and invasion (IC₅₀ ~4.0 μM in PANC-1), suppressed invadopodia-mediated ECM degradation, downregulated MMP-2/9, induced TIMP-1, restored E-cadherin, and inhibited PI3K/Akt/NF-κB and mTOR/S6K signaling cascades.

Conclusion: PA and EPA β-amino acid conjugates display distinct but complementary anticancer mechanisms, with conjugate 5 acting as an apoptosis inducer and conjugate 20 as an anti-metastatic agent. Their ability to modulate PI3K/Akt/NF-κB signaling underscores their potential as promising leads for targeted pancreatic cancer therapy.

Keywords: Piperic acid conjugates; β-amino acids; Pancreatic cancer; PI3K/Akt/NF-κB signaling; Anticancer and anti-metastatic agents

How to cite this article: Shrivastava P, Upadhyay P, Swapna M, Madhavilatha B, Khatoon Y, Peela M, Sharma S, Sonu, Synthesis and Biological Evaluation of Piperic Acid and 4-Ethylpiperic Acid β-Amino Acid Conjugates as Anticancer Agents Targeting PI3K/Akt/NF-κB Signaling in Pancreatic Cancer Cells. Int J Drug Deliv Technol. 2026;16(4s): 821-830; DOI: 10.25258/ijddt.16.4s.95

Source of support: Nil

Conflict of interest: None