PK-11195 was first discovered by Pharmuka Laboratories. It was found to be antagonist of the Translocator Protein (TSPO) with potential for development in a number of conditions including cancer models, cardiac ischemia, seizures, depression, and anxiety. PK-11195 has been studied extensively in vitro and in animal models. In phase I clinical trials no anti-inchemic effects were found after drug administration. A tritium [3H] labeled and a C-11 labeled version of PK-11195 are both used diagnostically as PET imaging compounds.

GSK-9089 (also known as DY131, N-(4-(Diethylaminobenzylidenyl)-N'-(4-hydroxy benzoyl)-hydrazine) is a novel selective agonist at estrogen-related receptors ERRβ and ERRγ, that displays minimal activity at ERRα, ERα and ERβ at concentrations up to 30 μM. DY131 inhibits growth in a diverse panel of prostate and breast cancer cell lines, causing cell death that involves the p38 stress kinase pathway and a bimodal cell cycle arrest.

(R)-Aminoglutethimide is R-isomer of racemate anti-steroid drug Aminoglutethimide, marketed by Novartis for the treatment of Cushing syndrome and other conditions. (R)-Aminoglutethimide was shown to more active than (S)-isomer in inhibiting corticosteroid release in rats, more potent in inhibiting aromatization of testosterone by human placental microsomes. (R)-Aminoglutethimide was investigated in a clinical trial against breast cancer, where it was found to enhance the clearance rate of plasma estrone sulfate.

PD-166866 is a member of a new structural class of tyrosine kinase inhibitors, the 6-aryl-pyrido[2,3-d]pyrimidines. PD 166866 is an inhibitor of FGFR1. PD166866 might be used in the control of fibrotic proliferative diseases, as well as in other tumor pathologies. PD166866 inhibits proliferation and triggers anoikis in FGFR1-amplified breast cancer cell lines. Mechanistic study reveals that PD166866 induces autophagy through repressing Akt/mTOR signaling pathway.

BMS-345541 is a highly selective inhibitor of I kappa B kinase that binds at an allosteric site of the enzyme and blocks NF-kappa B-dependent transcription in mice. BMS-345541 was identified as a selective inhibitor of the catalytic subunits of IKK (IKK-2 IC(50) = 0.3 uM, IKK-1 IC(50) = 4 uM). A binding model is proposed in which BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, which then affects the active sites of the subunits differently. BMS-345541 was shown to have excellent pharmacokinetics in mice, and peroral administration showed the compound to dose-dependently inhibit the production of serum tumor necrosis factor alpha following intraperitoneal challenge with lipopolysaccharide. BMS-345541 is effective against NF-kappa B activation in mice and represents an important tool for investigating the role of IKK in disease models. BMS-345541 blocks both joint inflammation and destruction in collagen-induced arthritis in mice.

BAY 61-3606 is a potent inhibitor of spleen tyrosine kinase (Syk) which is playing essential roles in receptors for Fc portion of immunoglobulins and B cell receptor complex signaling in various inflammatory cells. In addition, BAY61-3606 could inhibit the inhibitor of nuclear factor kappa B kinase (IKK-alpha) kinase activity. The compound is able to inhibit neoplastic phenotype of leukemia cells as well as of colon and breast cancer cells in vitro. BAY 61-3606 also exrets antiinflammatory and antiallergic properties in animal models.

Cucurbitacin D is a plant steroid with anticancer activity. Cucurbitacin D treatment of cervical cancer cells arrested the cell cycle in G1/S phase, inhibited constitutive expression of E6, Cyclin D1, CDK4, pRb, and Rb and induced the protein levels of p21 and p27. Cucurbitacin D also inhibited phosphorylation of STAT3 at Ser727 and Tyr705 residues as well as its downstream target genes c-Myc, and MMP9. In addition, Cucurbitacin D could be used as a useful compound to treat adriamycin-resistant patients with breast carcinoma.

LDC1267 preferentially inhibits TAM tyrosine kinase receptors Tyro3, Axl and Mer at low nanomolarity. LDC1267 conferred therapeutic potential, efficiently enhancing anti-metastatic natural killer (NK) cells activity. In vivo the compound markedly reduced murine mammary cancer and melanoma metastases dependent on NK cells.

Gliotoxin is a potent crystalline antibiotic substance produced during the growth of the imperfect fungus Gliocladium jimbriatum. It is a natural mycotoxin with immunosuppressive and antimicrobial activity. Gliotoxin acts as NOTCH2 transactivation inhibitor in human neoplasias. It induced growth inhibition and apoptosis in multiple colorectal cancer cell lines with mutations of the Wnt signaling pathway. Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats. Gliotoxin is a dual inhibitor of farnesyltransferase and geranylgeranyltransferase I with pronounced antitumor activity and favorable toxicity profile against breast cancer in vitro and in vivo.

23-epi-26-deoxyactein (formerly 27-deoxyactein), is the most abundant triterpene glycosides of black cohosh, inhibits growth of the MCF7 human breast cancer cells and induces cell cycle arrest at G1 and might eventually be useful in the prevention or treatment of breast cancer. Also was investigated the mechanism of action of 23-epi-26-deoxyactein, and was shown that 23-epi-26-deoxyactein decreased IFNγ-induced iNOS mRNA and NO production in brain microglial cells.