Embelin is a benzoquinone derivative found in Ardisia japonica which is a plant native to eastern Asia. It is used as an anti-cancer compound as well as an anti-inflammatory. Embelin has also been exhibited anthelminthic properties against cestode parasites.

In oncology research, embelin has been used to disrupt X-linked inhibitor of apoptosis (XIAP) activity. Embelin binds the Baculovirus IAP Repeat 3 (BIR3) domain on XIAP and subsequently disrupts apoptosis regulation. Inactivation of BIR3 allows proteins caspase-9 and Diablo homologs/Smac proteins to freely promote apoptotic pathways.

Embelin has also been used to quell inflammatory responses by inhibiting eicosanoid synthesis.It has been shown that embelin targets eicosanoid synthesizing proteins 5-lipoxygenase (5-LO) and microsomal prostaglandin E2 synthase (MPGES). Embelin has also been shown to disrupt eicosanoid synthesis through XIAP suppression.

EGCG has been shown to have a broad spectrum of antibacterial activity against gram positive and some gram negative bacteria. It is used synergistically with penicillin binding protein inhibitors because both target peptidoglycan on the cell wall. While the exact mechanism is not known, research on EGCG activity indicates bacterial cell wall damage by direct peptidoglycan binding.

Erlotinib HCl is an anti-cancer agent targeting epidermal growth factor receptor (EGFR) tyrosine kinase ATP binding sites, which are commonly overexpressed and sometimes mutated in a variety of cancers. Erlotinib prevents the formation of EGFR homodimers leading to suppression of signal transmittance and tumor growth inhibition. Additionally, erlotinib suppresses cyclin-dependent kinase 2 (Cdk2). It has been shown to be effective against non-small cell lung cancer and pancreatic cancer.

Gefitinib is an anti-cancer agent similar to erlotinib. It functions through inhibiting the overexpressed or mutated epidermal growth factor receptor (EGFR) by binding its ATP binding site. Overexpression and mutation of EGFR are common in cancer cell lines and may lead to uncontrolled proliferation through the Ras signaling cascade. Gefitinib has been shown to induce tumor cell apoptosis in HaCaT cells, KG-1 cells, P39 cells, and CD34+ myeloblasts. Additionally, it has been shown to promote keratinocyte apoptosis.

Germacrone is an essential oil extracted from Rhizoma curcuma and has been used as an anti-cancer and anti-viral agent. It has been shown to eliminate hepatic and breast cancer cell lines by inhibiting cyclin dependent kinase 2 (CDK2) activity. It has also been shown to upregulate apoptotic protein expression.

Inhibition of viral replication by germacrone occurs early in the virus cycle. When used against influenza, germacrone inhibited in vivo and in vitro viral replication by inhibiting viral RNA and protein synthesis. This prevents viral replication after splicing DNA by removing the needed materials for proliferation.

Hydroxyurea is a compound used in anti-cancer research to inhibit DNA synthesis and in sickle cell research for ways to alleviate symptoms. It has been shown to be a potent inhibitor of ribonucleotide reductase which reduces ribonucleotides to deoxyribonucleotides.

In vivo research has shown hydroxyurea converting into a free radical nitric oxide which binds the active site of ribonucleotide reductase, ceasing further DNA synthesis. The mechanism of nitric oxide release from hydroxyurea is not well understood.

Hydroxyurea has also been shown to alleviate sickle cell anemia through its conversion to nitric oxide in vivo. Nitric oxide alleviates endogenous nitric oxide loss, caused by hemolysis, and stimulates soluble guanylate cyclase (sGC) activity which will signal fetal hemoglobin production.

Icariin is a prenylflavonoid with anti-cancer properties and is studied for its diverse signaling effects observed in vivo. It has been documented to stimulate pathways that induce osteogenesis, decrease inflammation and promote angiogenesis.

Icariin has been shown in vivo to induce mice bone formation through upregulating runt-related transcription factor 2 (Runx2) genes and increasing bone morphogenic protein expression. These prompt osteogenic differentiation and bone development. Also, icariin invokes marrow stromal cell proliferation via increased alkaline phosphatase activity.

In vitro, icariin has been used to induce apoptosis by generating reactive oxygen species (ROS) and stimulating c-Jun N-terminal kinase (JNK) activity. Both of these apoptosis inducing processes compromise mitochondrial membranes to release cytochrome c. The generation of ROS causes direct damage to the membrane while JNK prompts downstream molecules to form pores in mitochondrial membranes.

Icariin has also been shown to inhibit nuclear factor-κB (NF-κB) expression, decreasing cytokine production. Additionally, icariin innervates phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) cell cycle pathways. The PI3K/AKT pathway has been demonstrated in vitro to induce angiogenesis, following the addition of icariin.

Icaritin is a prenylflavonoid derivative of icariin (Goldbio # I-215) and has been used for oncology research, to influence bone formation and displays neuroprotective effects. Applications in oncology and neurology research have been related to the activity of icaritin on estrogen receptors.

Within the field of cancer research, icaritin has been shown to act as an agonist and antagonist on estrogen receptors in vivo which was based upon concentration in different cancer lines. Icaritin was shown in vitro to sustain extracellular signal–regulated kinase (ERK) activity through stimulating estrogen receptors. Prolonged ERK activation arrested the cell cycle in the G2 stage and subsequently triggered apoptosis. Anti-cancer activity of icaritin has also been observed to occur in estrogen receptor negative cancer cells, showing an estrogen receptor independent pathway.

For Alzheimer’s research, icaritin has been investigated for attenuating cytotoxic effects caused by β-Amyloid proteins. While the mechanism for neuroprotection has not been elucidated, icaritin was shown to possibly exert these effects through mitogen-protein kinase (MAPK)/ERK cell signaling pathways.

Icaritin exerts an osteogenic effect in vivo by forming a bioactive scaffold that promotes bone growth while also increasing alkaline phosphatase (ALP) activity. It is also used to inhibit osteoclast differentiation and activity through suppression of receptor activator of nuclear factor kappa-B ligand (RANKL).

Icotinib hydrochloride or icotinib HCl, is a first generation inhibitor of tyrosine kinase epidermal growth factor receptor (EGFR-TK). It has been used in measuring the efficacy of novel anti-cancer compounds in vivo against non-small-cell lung cancers that formed advanced solid tumors. Icotinib reversibly inhibits EGFR-TK competitively by blocking the ATP-binding site on tyrosine kinase.

Ingenol mebutate (Ingenol-3-mebutate) is a hydrophobic diterpene ester extracted from the plant Euphorbia peplus. This compound is used in oncology research as an activator of the protein kinase C (PKC) family. Ingenol mebutate has been effective against basal cell carcinomas, squamous cell carcinomas and actinic keratosis.

Research on stimulation of PKC pathways by ingenol mebutate were shown to promote apoptosis, arrest cell growth and increase neutrophilic infiltration. Halting cell growth subsequently leads to apoptosis due to intracellular signals triggered from a lack of progression in the cell cycle. Ingenol mebutate diminished relapse rates of mice tumors in vivo and in vitro by inducing neutrophil recruiting and activating pathways. These pathways include releasing inflammatory cytokines interleukin 8 (IL8), interleukin 1 (IL1) as well as tumor necrosis factor alpha (TNF-α) which attract neutrophils to the inflammatory site.

Ixazomib citrate is a citrate salt that is a second generation proteasome inhibitor used for anti-cancer research. In vivo research has shown ixazomib citrate to hydrolyze into its active ixazomib form which reversibly inhibits 20S proteasomes in multiple myeloma cancer cells. Ceasing this enzyme’s activity has been shown to decrease angiogenesis, induce apoptotic pathways and upregulate tumor suppressor genes.