Androgenic alopecia (AA) is a condition that most commonly affects adult men and is caused by an increase in the hormone dihydrotestosterone (DHT) in the hair follicles. Anti-alopecia drugs should be discovered for hair follicles to enter the anagen growth phase. Therefore, this study evaluated the hair growth-promoting activity of Noni fruit’s water, ethyl acetate, n-hexane fractions, and sub-fractions from the active fraction in the alopecia male white rabbit model. The Matias method was modified by inducing rabbits using DHT for 17 days, followed by topical application of Noni fruit solution for 21 days. Meanwhile, hair growth was evaluated by histological observation of the follicular density and the anagen/telogen (A/T) ratio in skin tissue. In the first stage, five groups of male white rabbits were studied to obtain the active fraction; DHT+Minoxidil as standard, DHT+vehicle (NaCMC 1%), DHT+FW, DHT+FEA, and DHT+FH. The FEA as the active fraction was followed by open-column chromatography separation (DCM:Methanol) with a gradient of 10% to produce sub-fractions. In the second stage, the six main sub-fraction groups of male rabbits studied were DHT+FEA-1 to DHT+FEA-6. The follicular density of groups FEA-3 was 78.00 ± 1.52 compared with 31.55 ± 1.64 and 80.12 ± 1.02 in the Vehicle and Minoxidil groups. Additionally, group FEA-3 showed large numbers of anagen follicles with an A/T ratio of 1.64/1 compared to the vehicle group of 1/1.50 and 1.39/1 for Minoxidil control. Group FEA-3 was identified by LC-MS/MS-QTOF, followed by molecular docking to the androgen receptor (PDB: 4K7A), causing alopecia. The results showed that three alkaloid compounds with skeleton piperazine and piperidine, namely (compounds 2 (−4.99 Kcal/mol), 3 (−4.60 Kcal/mol), and 4 (−4.57 Kcal/mol)) had a binding affinity similar to Minoxidil, with also has alkaloid skeleton piperidine–pyrimidine (−4.83 Kcal/mol). The dynamic behavior showed the stability of all androgen receptor compounds with good RMSD, SMSF, and SASA values after being studied with 100 ns molecular dynamics (MD) simulations. This study produced a common thread in discovering a class of alkaloid compounds as inhibitors of androgen receptors that cause alopecia.

The use of phenotypic assay requires laborious work to culture HIV isolates to observe the phenotypic change of the virus in the presence of antiretroviral drugs. The genotypic approach may rely on the secondary data of documented mutations that are responsible for phenotypic alterations to antiretroviral-resistant HIV. HIV genomes were extracted from patients’ plasma, which was subsequently subjected to RT-PCR and Sanger sequencing. The obtained HIV genome sequencing data were analyzed for mutation detection. Three-dimensional (3D) structures of mutant HIV protease were constructed using FoldX software. The binding affinity of the mutant HIV protease with protease inhibitor drugs (Saquinavir, Ritonavir, Nelfinavir, Indinavir, and Lopinavir) was analyzed using AutoDock Vina. There were 90 patients involved in this study. The patients attended the Voluntary Counseling Test (VCT) of Mitra Masyarakat Hospital in Mimika, Papua, Indonesia. Among recruited subjects, the HIV genomes corresponding to the protease-encoded gene of 30 patients were successfully sequenced. There was only one patient (RSMM_70) infected with HIV harboring minor mutations (L10V, I15V, M36I, and R41K) in the protease-encoded gene that was not a new finding mutation. The 3D structure showed that the hydrophobicity and stability of mutant HIV protease were different from the wild genotype. Docking analysis showed decreasing binding affinity of the mutant HIV protease to the protease inhibitor drugs, which may lead to the alteration of inhibitory effectiveness. In silico docking, the analysis may provide an alternative approach to predict the effect of minor mutations in the HIV protease gene on the effectiveness of protease inhibitor drugs.