Androgenetic alopecia is the most common non-scarring hair loss in men. In genetically predisposed individuals, androgens affect hair follicles by transforming terminal hair into vellus-like miniaturized hair. This process leads to gradual hair loss.

In addition, Tthe enzyme 5α-reductase (5AR) mediates the conversion of testosterone to dihydrotestosterone (DHT). The 5AR family consists of three types: I, II, and III. These enzymes play a role in the metabolism of bile, androgens, and estrogens. Besides, type II 5AR is abundantly expressed in the prostate and hair follicles. Furthermore, men with pattern baldness often exhibit elevated type II 5AR activity along with increased DHT levels in the scalp. These findings support the significant roles of the type II isoenzyme and DHT in androgenetic alopecia. Therefore, Finasteride (MK-906), an orally active and competitive inhibitor of 5α-reductase, is very potential. Afterwards, it has an IC₅₀ of 4.2 nM for type II 5AR and is valuable in studies related to benign prostatic hyperplasia (BPH) and androgenetic alopecia (AGA).

Finasteride is an orally active 5α-reductase inhibitor with anti-myelofibrosis activity.

In vitro, Finasteride inhibits the type II 5α-reductase isoenzyme with 100-fold greater selectivity than the type I isoenzyme. Additionally, at a concentration of 25 µM, Finasteride reduces prostate-specific antigen (PSA) secretion and expression in LNCaP cells. It works by inhibiting the formation of complexes between the androgen receptor and steroid receptor-binding consensus in the promoter region of the PSA gene.

In vivo, Finasteride (0.1-0.5 mg/kg; p.o. once daily for 16 weeks) reduces prostatic size in dogs with BPH without adversely affecting semen quality or serum testosterone concentration. Moreover, Finasteride decreases prostatic diameter (20%), prostatic volume (43%), and serum DHT concentration (58%).

In summary, Finasteride is a potent 5α-reductase inhibitor, and is potential for research of hair loss, benign prostatic hyperplasia, and androgenetic alopecia (AGA).

References:

[1] Sirinarumitr K, et, al. J Am Vet Med Assoc. 2001 Apr 15;218(8):1275-80.

[2] Gupta AK, et al. J Dermatolog Treat. 2022 Jun;33(4):1938-1946.

[3] Wang LG, et al. Cancer Res. 1997 Feb 15;57(4):714-9.

Alzheimer’s disease (AD) is marked by a gradual decline in cognitive function and memory impairment. This decline significantly impacts the daily lives of patients. One widely accepted cause of AD is the cholinergic hypothesis, which suggests that the selective loss of cholinergic neurons in the basal forebrain leads to decreased choline levels. Moreover, cholinergic neurotransmitters are essential for regulating higher brain functions, including memory, learning, and cognition.

To address cholinergic dysfunction in AD, researchers have widely employed cholinesterase inhibitors as therapeutic interventions. Among these, Rivastigmine (ENA 713 free base) stands out as an orally active cholinesterase inhibitor that can penetrate the blood-brain barrier (BBB). Notably, it inhibits both butyrylcholinesterase (BChE) and acetylcholinesterase (AChE) with IC₅₀ values of 0.037 μM and 4.15 μM, respectively.

As a classic cholinesterase inhibitor, Rivastigmine has been recommended as a first-line treatment for mild to moderate AD for decades. Furthermore, it is available in various forms, including oral capsules, transdermal patches, and nasal sprays. Thus, Rivastigmine provides multiple options for managing the symptoms of Alzheimer’s disease effectively..

Rivastigmine is a cholinesterase inhibitor for research of mild to moderate Alzheimer’s disease.

In vitro, Rivastigmine (24 μM for 24 hours) enhances neuronal morphology. It also increases the levels of proteins such as NSE, SNAP-25, and synaptophysin. Consequently, Rivastigmine has the potential to preserve both neuronal viability and structure.

In vivo, Rivastigmine (0.5-2.5 mg/kg; i.p.; administered 60 minutes before tests) significantly and dose-dependently improves behavioral impairments caused by Aluminum (100 mg/kg/day; i.p.). It enhances activity, learning, and memory in a dose-dependent manner. Notably, Rivastigmine (2.4 mg/kg, once a day, via intranasal administration) rapidly diffuses into the brain but is eliminated slowly, thus improving memory deficits associated with Alzheimer’s disease. Additionally, Rivastigmine inhibits collagen deposition and reduces the expression level of Aβ in models of Alzheimer’s induced by intra-hippocampal injection of Aβ1-42.

In summary, Rivastigmine is an orally active cholinesterase inhibitor, and improves memory deficits associated with Alzheimer’s disease.

References:

[1] Raafat A Abdel-Aal, et al. Eur J Pharmacol. 2011 Jun 1;659(2-3):169-76.

[2] Guo H, et al. Int J Pharm. 2024 Mar 5;652:123809.

[3] Bailey JA, et al. J Neurochem. 2010 Feb;112(4):843-53.

Product Name :
aconitase 2, mitochondrial