Recombinant Human AKR1C2

Background

AKR1C2, known as 3α-hydroxysteroid dehydrogenase, catalyzes the reduction of 5α-dihydrotestosterone (DHT) to 3α-androstanediol, thereby inactivating this potent androgen. AKR1C2 is a key regulator of androgen and neurosteroid metabolism, playing a crucial role in modulating androgen signaling in tissues such as the prostate, brain, and liver. Dysregulation of AKR1C2 is associated with androgen-driven diseases, including prostate cancer, where its activity can suppress DHT levels and attenuate androgen receptor signaling. AKR1C2 also metabolizes progesterone and other steroid intermediates, linking it to reproductive and neuroendocrine functions. Its role in neurosteroid metabolism influences processes like synaptic inhibition, neuroprotection, and stress responses in the brain. Overexpression of AKR1C2 has been reported in cancers and drug-resistant tumors, where it contributes to detoxifying reactive carbonyl species and reducing chemotherapeutic efficacy. As a result, AKR1C2 is considered a therapeutic target for prostate cancer and neurodegenerative disorders.