Hypoxanthine–guanine phosphoribosyltransferase (HGPRT (also commonly HPRT))

**Hypoxanthine–guanine phosphoribosyltransferase (HGPRT)** is an enzyme critical for the purine salvage pathway, facilitating the conversion of free purine bases (hypoxanthine and guanine) to their nucleotide forms (inosine monophosphate, guanosine monophosphate) using phosphoribosyl pyrophosphate (PRPP) as a ribose-phosphate donor[1][2][4]. It is encoded by the HPRT1 gene in humans and is widely expressed in tissues with high nucleotide turnover. HGPRT is essential for reutilizing purines from degraded nucleic acids, thus maintaining the cellular pools of nucleotides necessary for DNA and RNA synthesis[1][2][6]. Deficiency of HGPRT leads to Lesch–Nyhan syndrome, characterized by neurologic dysfunction, self-injurious behavior, hyperuricemia, and renal complications[1][4][6]. In pathogenic protozoa like *Plasmodium falciparum*, the enzyme also catalyzes xanthine salvage, thus sometimes referred to as HGXPRT. These differences are exploited in the development of antiparasitic therapies[5][7]. The enzyme is used as a selection marker in hybridoma and cell engineering technologies[1][4]. Its substrate analogues are important in cancer chemotherapy and immunosuppression[4][5][7]. **Note:** - The submitted name "hypoxanthine–guanine–xanthine phosphoribosyltransferase" is accurate only for some parasitic and microbial homologs. In standard human/vertebrate biochemistry, the canonical target is "Hypoxanthine–guanine phosphoribosyltransferase (HGPRT, HPRT1)"[1][2][5][7]. - If your target is the human or mammalian enzyme, use "Hypoxanthine–guanine phosphoribosyltransferase." For *Plasmodium* or similar organisms, "hypoxanthine–guanine–xanthine phosphoribosyltransferase" (HGXPRT) is appropriate[5][7].

Other names

HPRTHGPRTHypoxanthine phosphoribosyltransferaseGuanine phosphoribosyltransferasePhosphoribosyltransferase, hypoxanthine-guanine(For parasites: often HGXPRT or Hypoxanthine–guanine–xanthine phosphoribosyltransferase)

Substrate analogues (e.g., 6-mercaptopurine, 6-thioguanine) act as **antimetabolites**, competing with natural substrates, incorporated to disrupt nucleic acid synthesis, or poison purine salvage. Inhibitors for parasitic HGXPRT (malaria, trypanosomiasis) work by **enzyme inhibition**, blocking nucleotide salvage, which leads to parasite death.