Nitisinone | Tyrosine metabolism inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 50 mg | $25.00 | ||
| 250 mg | $95.00 |
Nitisinone (104206-65-7) is an inhibitor of 4-Hydroxyphenylpyruvate dioxygenase (HPPD; IC50 = 40 nM1 and 173 nM2) and is in clinical use for the treatment of hereditary tyrosinemia type 13. CD13+ cancer stem cells (CSCs) are dependent on aerobic metabolism of tyrosine – Nitisinone inhibition of tyrosine metabolism results in lowered availability of acetyl-CoA and fumarate for use in the citric acid cycle causing these CSCs to enter cell cycle, decreasing self-renewal, and making them more susceptible to chemotherapy.4 Nitisinone is a potential treatment option for cancers that rely on tyrosine metabolism.
References/Citations:
- Ellis et al. (1995), Inhibition of 4-hydroxy-phenylpyruvate dioxygenase by 2-(2-nitro-4-trifluoromethylbenzoyl)-cyclohexane-1,3-dione and 2-(2-chloro-4-methanesulfonylbenzoyl)-cyclohexane-1,3-dione; Toxicol. Appl. Pharmacol., 133 12
- Laschi et al. (2016), Inhibition of para-hydroxyphenylpyruvate dioxygenase by analogues of the herbicide nitisinone as a strategy to decrease homogentisic acid levels, the causative agent of alkaptonuria; Chem. Med. Chem., 11 674678
- McKiernan (2006), Nitisinone in the treatment of hereditary tyrosinaemia type 1; Drugs, 66 743
- Sun et al. (2020), Activation of Tyrosine Metabolism in CD13+ Cancer Stem Cells Drives Relapse in Hepatocellular Carcinoma; Cancer Res. Treat., 52 604
NMR (Conforms)
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Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
Nitisinone (104206-65-7) is an inhibitor of 4-Hydroxyphenylpyruvate dioxygenase (HPPD; IC50 = 40 nM1 and 173 nM2) and is in clinical use for the treatment of hereditary tyrosinemia type 13. CD13+ cancer stem cells (CSCs) are dependent on aerobic metabolism of tyrosine – Nitisinone inhibition of tyrosine metabolism results in lowered availability of acetyl-CoA and fumarate for use in the citric acid cycle causing these CSCs to enter cell cycle, decreasing self-renewal, and making them more susceptible to chemotherapy.4 Nitisinone is a potential treatment option for cancers that rely on tyrosine metabolism.
References/Citations:
- Ellis et al. (1995), Inhibition of 4-hydroxy-phenylpyruvate dioxygenase by 2-(2-nitro-4-trifluoromethylbenzoyl)-cyclohexane-1,3-dione and 2-(2-chloro-4-methanesulfonylbenzoyl)-cyclohexane-1,3-dione; Toxicol. Appl. Pharmacol., 133 12
- Laschi et al. (2016), Inhibition of para-hydroxyphenylpyruvate dioxygenase by analogues of the herbicide nitisinone as a strategy to decrease homogentisic acid levels, the causative agent of alkaptonuria; Chem. Med. Chem., 11 674678
- McKiernan (2006), Nitisinone in the treatment of hereditary tyrosinaemia type 1; Drugs, 66 743
- Sun et al. (2020), Activation of Tyrosine Metabolism in CD13+ Cancer Stem Cells Drives Relapse in Hepatocellular Carcinoma; Cancer Res. Treat., 52 604
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1-855-FOCUS21
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