Benzquercin is a member of flavones. Experiments on mice have shown that compound decreased morphological disorders of the connective tissue of lathyritic mice and the vascular permeability was close to normal controls.

Tetroquinone (Tetrahydroxy-1,4-benzoquinone, tetrahydroxy-p-benzoquinone, tetrahydroxybenzoquinone) is cyclohexadiene derivative with four hydroxyl groups and two ketone groups in opposite (para) positions, with potent prooxidant activity. The exposure of exponentially growing cultures to Tetroquinone, in the presence of Ca2+, caused a dose-dependent inhibition of cell growth and DNA synthesis. The chemical reactivity of Tetroquinone is strongly similar to those of physiological polyphenols, such as catechols and catecholamines. Despite their physiological and pharmacological roles, these compounds may, in addition, present toxicological properties due to their ability to autoxidize generating ROS and quinones Similar to catechols, the OH-substituents confer to Tetroquinone the ability to autoxidize readily in neutral aqueous solutions generating intermediate superoxide anion radicals, semiquinone radicals, and the corresponding quinone. The compound can be synthesized from glyoxal or from myo-inositol (phytic acid), a natural compound widely present in plants.

Cytidine is a substrate of the uridine-cytidine kinase and is a part nucleic acids. It can serve as a substrate for the salvage pathway of pyrimidine nucleotide synthesis, as a precursor of the cytidine triphosphate (CTP) needed in the phosphatidylcholine (PC) and phosphatidylethanolamine (PE) biosynthetic pathway. Cytidine was also used under the brand name posilent in Germany for the treatment of muscular, accommodative, and nervous eye disorders.

Sanguinarine is an extract of the bloodroot plant Sanguinaria canadensis, a member of the poppy family. It is an inhibitor of protein phosphatases PP1, PP2C and PP2B in vitro. Also inhibits mitogen-activated protein kinase phosphatase-1 (MKP-1) and other enzymes. Sanguinarine exerts a protective effect in cerebral ischemia, and this effect is associated with its anti-inflammatory and anti-apoptotic properties. It was clinically tested as an agent against gingivitis and tooth plaques.

Staurosporine is an alkaloid isolated from the culture broth of Streptomyces staurosporesa. It exerts antimicrobial, hypotensive, and cytotoxic activity. The main biological activity of staurosporine is the inhibition of protein kinases through the prevention of ATP binding to the kinase. This is achieved through the stronger affinity of staurosporine to the ATP-binding site on the kinase. Staurosporine is a prototypical ATP-competitive kinase inhibitor in that it binds to many kinases with high affinity, though with little selectivity. It is a potent, cell permeable protein kinase C inhibitor with an IC50 of 0.7 nM. At higher concentration (1-20 nM), staurosporine also inhibits other kinases such as PKA, PKG, CAMKII and Myosin light chain kinase (MLCK). At 50-100 nM, it is a functional neurotrophin agonist, promoting neurite outgrowth in neuroblastoma, pheochromocytoma and brain primary neuronal cultures. At 0.2- 1 uM, staurosporine induces cell apoptosis. Staurosporine is also a potent GSK-3β inhibitor with a reported IC50 value of 15 nM. In research, staurosporine is used to induce apoptosis. It has been found that one way in which staurosporine induces apoptosis is by activating caspase-3. Staurosporine was discovered to have biological activities ranging from anti-fungal to anti-hypertensive. The interest in these activities resulted in a large investigative effort in chemistry and biology and the discovery of the potential for anti-cancer treatment. Staurosporine induces apoptosis by multiple pathways and that the inhibition of more than one kinase is responsible for its potent activity. Because the mechanism of action of staurosporine is distinct from traditional anticancer drugs, this may warrant further preclinical evaluations of the antitumor potential of new staurosporine derivatives either alone or in combination with death ligands or conventional chemotherapeutic drugs.