Table 3.

List of some plant-derived antineoplastic lead compounds currently in use and currently in clinical trials [81, 82].

	Source of plant	Specific mechanism of actions of the lead compounds
Antineoplastic lead compounds currently in use
Vinblastine, Vincristine	Catharanthus roseus	Bind to the microtubulin site in the β-subunit and disrupt the assembly of microtubules in mitosis [83]
Taxol	Taxus brevifolia	Binds to the taxane site as a microtubule stabilizer and interfering with the normal breakdown of microtubules during cell division [84]
Etoposide	Podophyllum peltatum	Binds to tubulin and interferes with the formation of spindles in mitosis [85]
Camptothecin, irinotecan, and topotecan	Camptotheca acuminata	Arrest the cell cycle at the S-phase by inhibiting the activity of topoisomerase I, leading to the inhibition of DNA replication and transcription [86, 87]
Antineoplastic lead compounds currently in clinical trials
Homoharringtonine	Harringtonia cephalotaxus	Inhibits protein synthesis and blocking cell-cycle progression [88], promotes apoptosis, and inhibits protein synthesis at the ribosomal level [89, 90]
Curcumin	Curcuma longa	Induces apoptosis and inhibits the proliferation of a variety of malignant cells and is involved in the regulation of combined signaling pathways at multiple levels by acting on various targets including modulation of gene transcription factors (NFκB, p53, and AP-1), growth factors and their receptors (PDGF, EGF, and VEGF), cell surface adhesion molecules (E-cadherin, β-cadenin), and protein kinases (CDKs, EGFR, PKC, and p38 MAPK) [91, 92]
Resveratrol	Vitis vinifera, Morus alba, and Arachis hypogaea	Inhibits the growth of cancer cells and induces apoptosis by acting at multiple cellular targets, including activation of p53, inhibiting 10 otulins, 10 genases, and cytochrome P450 enzymes, and activating AMP-activated kinase (AMPK) [93–95]
Flavopiridol	Amoora rohituka	Exhibits apoptosis induction [96], inhibits the activity of cyclin-dependent kinases (CDKs) by competing with ATP at their nucleotide binding sites, and causes cell cycle arrest at either the G1 or G1/M phases [97]