For results for completed and on-going clinical trials in ovarian cancer for all drugs in a specific category, click on the drug category (e.g., Angiogenesis Inhibitors) on the left. To see only results for specific drugs in a class, click on the drug class for the drugs that interest you. For a schematic diagram of cell growth and survival pathways that these drugs inhibit, please scroll to the bottom of the page.
|DNA DAMAGE REPAIR PATHWAY INHIBITORS||PARP (Poly ADP-ribose Polymerase)||Niraparib (Zejula™)
|ANTIBODY (and other) TARGETED DRUG CONJUGATES||Antibody Drug Conjugates (ADC)
Targeting Mesothelin, MUC16, FRalpha,
|ANGIOGENESIS INHIBITORS||VEGF, DLL4 Antagonists||Bevacizumab (Avastin™)
|VEGFR, PDGFR Inhibitors||Cediranib
|ANTI-HORMONE THERAPY||Aromatase Inhibitors
|SIGNALING PATHWAY INHIBITORS||PI3K/AKT/mTOR Pathway
Targeting PI3Kalpha, pan-PI3K, mTOR, TORC1/2
|CELL CYCLE INHIBITORS||CDK4/6 Inhibitors||Palbociclib (Ibrance™)|
Targeting CTLA-4, PD-1, PD-L1
|Immune Cell Stimulators
Targeting tumor-associated antigens, Survivin, TGFbeta, NY-ESO-1
Targeting FRalpha, CA125
This diagram shows some of the key cell signaling pathways that are affected by genetic mutations or alterations found in ovarian cancers. The names of proteins encoded by the genes involved in various steps of each pathway are shown. Some proteins promote (indicated by an arrow) a particular step in the pathway and spur cell growth. Other proteins inhibit (indicated by the perpendicular symbol) a step in the pathway and prevent cells from growing and dividing in an uncontrolled way. Some genetic mutations/alterations result in a protein that is more active than it would normally be (shown in green), while others cause the protein to be less active (shown in red). A more active protein that stimulates cell growth or decreased activity of a protein that inhibits these processes can both lead to the uncontrolled growth seen in cancers.