Alzheimer's disease, a debilitating degenerative disorder, poses a formidable challenge in terms of treatment, with a projected surge in the number of afflicted individuals annually. The imperative quest for novel anti-Alzheimer's compounds derived from natural sources is underscored by the urgency to address this escalating health crisis. Austricin, identified in langsat kombucha, emerges as a promising candidate due to its demonstrated affinity for the muscarinic acetylcholine receptor M1 and anti-inflammatory properties. In this study, we conduct an extensive validation of austricin's potential through assessments of blood–brain barrier permeability, absorption, distribution, metabolism, and excretion. Additionally, we explore its binding capabilities with the pivotal protein steril-sulfatase, identified as a primary target in Alzheimer's pathology. Comparative analyses are performed with established compounds, donepezil and galantamine. Analysis reveals that austricin successfully traverses the blood–brain barrier (LogBBB -0.19498) with a solubility of 3.54e+00 mg/ml, high gastrointestinal absorption, and Lipinski's Rule of Five compliance. Importantly, it exhibits a bioavailability score of 0.55 and a synthetic accessibility of 4.60, establishing its potential as a viable drug candidate. The compound shows no substrate inhibition for major cytochrome P450 enzymes (CYP1A2, CYP2C19, CYP2C9, CYP2D6, and CYP3A4). Furthermore, molecular docking analyses reveal austricin's superior ΔG-binding affinity (-7.9 kcal/mol) compared to donepezil (7.4 kcal/mol) and galantamine (7.2 kcal/mol) for steril-sulfatase. While these findings suggest austricin's promise as an anti-Alzheimer's compound, further investigations on key Alzheimer's-associated proteins and in vitro testing are indispensable for conclusive validation and development. This study provides a foundation for the potential therapeutic application of austricin, paving the way for subsequent experimental endeavors and clinical investigations in the pursuit of effective Alzheimer's treatments.