For research use only. Not for therapeutic Use.
Pivalyloxymethyl butyrate（Cat No.:M024304）is a versatile chemical compound used primarily in the pharmaceutical industry as a prodrug linker and protective group. It facilitates the delivery of active pharmaceutical ingredients (APIs) by improving their bioavailability and stability. This compound enhances the pharmacokinetic properties of drugs, enabling more effective therapeutic results. Additionally, its incorporation into drug molecules can help protect against premature metabolism and degradation, allowing for sustained and controlled release. Pivalyloxymethyl butyrate is essential for optimizing drug formulation and enhancing medicinal compound efficacy in research and development.
| Catalog Number | M024304 |
| CAS Number | 122110-53-6 |
| Molecular Formula | C10H18O4 |
| Purity | ≥95% |
| Target | HDAC inhibitor |
| Storage | -20°C |
| IUPAC Name | butanoyloxymethyl 2,2-dimethylpropanoate |
| InChI | InChI=1S/C10H18O4/c1-5-6-8(11)13-7-14-9(12)10(2,3)4/h5-7H2,1-4H3 |
| InChIKey | GYKLFBYWXZYSOW-UHFFFAOYSA-N |
| SMILES | CCCC(=O)OCOC(=O)C(C)(C)C |
| Reference | 1:Mol Pharmacol. 2000 Jul;58(1):27-36. Anticancer derivative of butyric acid (Pivalyloxymethyl butyrate) specifically potentiates the cytotoxicity of doxorubicin and daunorubicin through the suppression of microsomal glycosidic activity.Niitsu N,Kasukabe T,Yokoyama A,Okabe-Kado J,Yamamoto-Yamaguchi Y,Umeda M,Honma Y, PMID: 10860924 </br><span>Abstract:</span> Pivalyloxymethyl butyrate (AN9) is an anticancer derivative of butyric acid. In this study, doxorubicin (DXR) and AN9 synergistically inhibited the growth of lymphoma and lung carcinoma cells, whereas there was no synergy between AN9 and antimetabolites. AN9 did not affect the intracellular uptake of DXR. Among anthracyclines and their derivatives, the synergistic effect was prominent in compounds with a daunosamine moiety, suggesting that AN9 may affect the catabolism of these compounds. The degradation of DXR in the extract from AN9-treated cells was much less than that in extract from untreated cells. AN9 did not directly inhibit the enzyme activity but rather suppressed expression of the enzyme. With respect to the expression of drug resistance-related genes, there was no significant difference between untreated and AN9-treated cells. However, AN9 significantly down-regulated the levels NADPH-cytochrome P450 reductase and DT-diaphorase mRNA in the presence of DXR but not the level of xanthine oxidase mRNA. The enhancement of the sensitivity to anthracyclines was closely associated with the suppression of the mRNA expression. |
