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L-Histidinol dihydrochloride

MCE China：L-Histidinol dihydrochloride

Brand：MedChemExpress (MCE)

Cat. No.HY-W014233

CAS：1596-64-1

Purity：98.0%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：L-Histidinol dihydrochloride is an orally active histidyl-tRNA synthetase inhibitor. L-Histidinol dihydrochloride interferes with the initiation stage of protein synthesis, thus affecting cell proliferation and metabolism. L-Histidinol dihydrochloride has the effect of modulating the sensitivity of tumor cells to chemotherapeutic agents. L-Histidinol dihydrochloride reduces the toxicity of certain chemotherapeutic agents to normal tissues and enhance the sensitivity of tumor cells to chemotherapeutic agents.

In Vitro：L-histidinol (1-15 mM; 4 h pretreatment) dihydrochloride potentiates hyperthermic cell (HeLa and S-180)-killing in-vitro[1]. L-histidinol (3 mM; 2 h) dihydrochloride inhibits protein and ribosomal RNA synthesis in mouse L cells[2]. L-histidinol (1-3 mM; 24 h) dihydrochloride shows a modest, dose-dependent toxicity to cultured P815 mastocytoma cells[3]. L-histidinol (3 mM; 48 h) dihydrochloride, when combined with different anticancer drugs, reverses the multidrug-resistance attribute of CHRC5 cells[4]. L-histidinol (1 mM; 24 h) dihydrochloride inhibits the proliferative responses induced by Con A and LPS (HY-D1056) in cultured mouse spleen cells[5].

In Vivo：L-Histidinol (5 mg/injection; i.p.; administered at -2, 0, 2, 4, and 6 h) dihydrochloride, when combined with ara-C (HY-13605) or FUra, eliminates their bone marrow toxicity in DBA/2J mice and enhances the eradication of intraperitoneal P815 mastocytoma cells[3]. L-Histidinol (250 mg/kg; i.p.) dihydrochloride, in combination with BCNU (HY-13585), improves the treatment effect of P388 leukemia in DBA/2J mice, increasing the median survival time and the number of 60-day survivors[6]. L-Histidinol dihydrochloride (7 mg/mouse; i.p.; 4 consecutive days a week, with 5 doses at 2-h intervals; for 3 weeks) significantly inhibits tumor growth in CD8F1 breast tumor mice[7]. L-Histidinol (100 mg/kg; i.p.; once every 2 h for 5 times; starting 2 h before Cisplatin administration) dihydrochloride reduces Cisplatin (HY-17394)-induced nephrotoxicity in rats and protects renal function[8]. L-Histidinol (0.5%, p.o., drinking water, 3 days before Ifosfamide administration and daily thereafter) dihydrochloride attenuates Fanconi syndrome induced by Ifosfamide (HY-17419) in rats[9].

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References：

[1]. Kohnoe S, et al. L-histidinol potentiates hyperthermic cell-killing in-vitro. Int J Oncol. 1993 Nov;3(5):835-9.

[2]. https://pubmed.ncbi.nlm.nih.gov/21573440/

[3]. Warrington RC, et al. Effects of L-histidinol on the susceptibility of P815 mastocytoma cells to selected anticancer drugs in vitro and in DBA/2J mice. J Natl Cancer Inst. 1987 Jun;78(6):1177-83.

[4]. Warrington RC, et al. Reversal of the multidrug-resistant phenotype of Chinese hamster ovary cells by L-histidinol. J Natl Cancer Inst. 1989 May 10;81(10):798-803. doi: 10.1093/jnci/81.10.798.

[5]. Warrington RC, et al. L-histidinol protection against cytotoxic action of cytosine arabinoside and 5-fluorouracil in cultured mouse spleen cells. J Natl Cancer Inst. 1982 Feb;68(2):279-86.

[6]. Zaharko D, et al. L-histidinol: preclinical therapeutic studies in combination with antitumor agents and pharmacokinetic studies in mice. Cancer Res. 1992 Jul 1;52(13):3604-9.

[7]. Stolfi RL, et al. Chemotherapeutic activity of L-histidinol against spontaneous, autochthonous murine breast tumors. Chemotherapy. 1990;36(6):435-40.

[8]. Badary OA, et al. Effect of L-histidinol on cisplatin nephrotoxicity in the rat. Nephron. 1997;77(4):435-9.

[9]. Badary OA. L-Histidinol attenuates Fanconi syndrome induced by ifosfamide in rats. Exp Nephrol. 1999 Jul-Aug;7(4):323-7.

[10]. Warrington RC, et al. L-histidinol improves the selectivity and efficacy of alkylating agents and daunomycin in mice with P388 leukaemia. Br J Cancer. 1989 Nov;60(5):652-6.