Decyl gallate 

Decyl gallate is an antifungal (fungal) agent. Decyl gallate downregulates the expression of the pro-apoptotic (apoptosis) protein Bak, upregulates the expression of the anti-apoptotic protein Bcl-2, and inhibits DNA damage. Decyl gallate disrupts ALG12-mediated N-glycosylation, overactivates the UPR pathway, and simultaneously reduces fungal cell wall enzyme activity, chitin levels, mitochondrial activity, budding ability, cell viability, and host cell adhesion capacity. Decyl gallate reduces inflammatory responses induced by fungal infection and disrupts fungal membrane structure. Decyl gallate can be used in studies related to paracoccidioidomycosis and invasive fungal infections^[1][2][3].

Co-incubation of Decyl gallate (G14) (0.012 µM; 24 h) with gp43 significantly reduces the level of gp43-induced DNA fragmentation in A549 lung cells, decreasing the DNA damage index from 45% to 35%^[1].
Co-incubation of decyl gallate (0.012 µM; 24-48 h) with gp43 significantly downregulates the gp43-induced expression of Bak protein and Bak mRNA in A549 lung cells. Compared with the group treated with gp43 alone, the Bak protein level decreases by 50% and the mRNA level decreases by 93.5% at 24 h, while the mRNA level decreases by 25.7% at 48 h^[1].
Co-incubation of Decyl gallate (0.012 µM; 24-48 h) with gp43 prevents the gp43-induced downregulation of Bcl-2 protein expression in A549 lung cells, and increases Bcl-2 mRNA expression by 2.73-fold at 24 h compared with untreated cells, thereby reversing the inhibitory effect induced by gp43^[1].
Decyl gallate (7 μg/mL; 48 h) alters the survival fitness of specific S. cerevisiae deletion mutants, among which mutants of the unfolded protein response (UPR) pathway are highly sensitive to it, and its action characteristics indicate that it targets the N-glycosylation pathway via ALG12^[2].
Decyl gallate (7 μg/mL; 3-24 h) hyperactivates the UPR pathway in S. cerevisiae strain YMJ003^[2].
Decyl gallate (0.5 μg/mL; 72 h) impairs the N-glycosylation pathway in P. lutzii strain 01, reduces glycosylase activity and cell wall glycosylation components, and simultaneously induces compensatory upregulation of related genes and unfolded protein response (UPR) pathway genes^[2].
Decyl gallate (0.5 μg/mL; 24-48 h) impairs mitochondrial activity, budding capacity, cell wall integrity, and cell viability of P. lutzii strain 01^[2].
Decyl gallate (0.5 μg/mL; 24 h) significantly reduces the adhesion of P. lutzii strain 01 to human lung epithelial A549 cells in vitro, without affecting fungal internalization or the viability of internalized fungi^[2].
Decyl gallate (0.5 μg/mL; 24 h) reduces nitrite production (a marker of inflammation) in RAW 264.7 macrophages stimulated with LPS (HY-D1056) or infected with P. lutzii, while enhancing the killing effect of macrophages against intracellular P. lutzii strain 01^[2].
Decyl gallate (0.002-62.5 mg/L; species-specific CLSI guidelines) potently inhibits and kills a variety of pathogenic fungi, with an MIC as low as 0.004 mg/L against *Paracoccidioides brasiliensis* isolates 18, 339, and *Paracoccidioides brasiliensis* 02. Moreover, the MFC values are consistent with the MIC values for most test strains^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

310.39

C₁₇H₂₆O₅

19198-75-5

O=C(C1=CC(O)=C(C(O)=C1)O)OCCCCCCCCCC

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Bernardi T, et al. Anti-apoptotic effects of decyl gallate on the induction of apoptosis in A549 pneumocytes by Paracoccidioides brasiliensis gp43. Med Mycol. 2017;55(8):890-894.

  [2]. de Paula E Silva ACA, et al. Decyl Gallate as a Possible Inhibitor of N-Glycosylation Process in Paracoccidioides lutzii. Antimicrob Agents Chemother. 2019 Oct 22;63(11):e01909-18.

  [3]. de Paula E Silva AC, et al. Antifungal Activity of Decyl Gallate against Several Species of Pathogenic Fungi. Evid Based Complement Alternat Med. 2014;2014:506273.