A Pyrone and Flavonoid Derivatives from Cryptocarya crassinervia and their Inhibitory Properties against Receptor Tyrosine Kinases

Dian Nugraheni (Organic Chemistry Division, Faculty of Mathematics and Natural Sciences, Institut Teknologi Bandung, Jalan Ganesha 10, Bandung 40132, Indonesia)
Elvira Hermawati (Organic Chemistry Division, Faculty of Mathematics and Natural Sciences, Institut Teknologi Bandung, Jalan Ganesha 10, Bandung 40132, Indonesia)
Hendra Helmanto (Research Center for Plants Conservation Botanic Garden and Forestry, National Research and Innovation Agency, Gedung Kusnoto, Jalan Ir. H. Juanda No. 18, Bogor 16122, Indonesia)
Dikhi Firmansyah (Organic Chemistry Division, Faculty of Mathematics and Natural Sciences, Institut Teknologi Bandung, Jalan Ganesha 10, Bandung 40132, Indonesia)
Yana Maolana Syah (Organic Chemistry Division, Faculty of Mathematics and Natural Sciences, Institut Teknologi Bandung, Jalan Ganesha 10, Bandung 40132, Indonesia)
Lia Dewi Juliawaty (Organic Chemistry Division, Faculty of Mathematics and Natural Sciences, Institut Teknologi Bandung, Jalan Ganesha 10, Bandung 40132, Indonesia)

Journal of Mathematical and Fundamental Sciences
Vol. 55 No. 3 (2024)

A new a-pyrone, i.e., cryptocrassinervione (1), and a new flavone glycoside, i.e., kaempferol-3-O-rhamnosyl-2-O-apiofuranoside (4), were isolated from EtOAc extract of Cryptocarya crassinervia leaves. Along with these compounds, two known flavone glycosides, namely afzelin (2) and quercitrin (3), were also isolated. The structures of the new compounds were determined based on NMR and mass spectral data. Compounds 1–4 were examined against eight receptor tyrosine kinases (RTKs) (EGFR, HER2, HER4, IGF1R, InsR, KDR, PDGFRα, and PDGFRβ), which showed that these compounds were moderately active against EGFR, with inhibition percentages of 55, 49, 41, and 44%, respectively. They were weakly active against HER2, with inhibitions of 17, 20, 18, and 16%, respectively. However, they were not active against the rest of the RTKs. Nevertheless, compounds 1–4 have potency as inhibitors of EGFR.