CMX001 (Brincidofovir; HDP-CDV) was developed as an orally active, lipophilic form of cidofovir (CDV); has enhanced activity in vitro and in vivo compared to CDV against certain herpesviruses, adenoviruses and orthopoxviruses.IC50 Value: 5.5 nM (EC50, in PDA at 7 dpi) [3]Target: anti-CMVCMX001 is currently in Phase II clinical studies for development as a therapeutic agent for human CMV, adenovirus and BK virus infections, as well as, for adverse events following smallpox vaccinations.in vitro: In PDA at 7 dpi, the CMX001 50% effective concentration (EC50) was 5.55 nM, the 50% cytotoxic concentration (CC50) was 184.6 nM, and the 50% selectivity index (SI50) was 33.3. The EC90 was 19.7 nM, the CC90 was 5,054 nM, and the SI90 was 256.1. In COS-7 cells, JCV replication was faster and the EC50 and EC90 were 18- and 37-fold higher than those in PDA, i.e., 0.1 μM and 0.74 μM (CC50, 0.67 μM; SI50, 6.7; CC90, 12.2 μM; SI90, 16.5) at 5 dpi [3].in vivo: CMX001 and CDV are equally efficacious at protecting mice from mortality following high ectromelia virus doses (10,000 x LD(50)) introduced by the intra-nasal route or small particle aerosol. Using CMX001 at a 10mg/kg dose followed by 2.5mg/kg doses every other-day for 14 days provided solid protection against mortality and weight loss following an intra-nasal challenge of (100-200) x LD(50) of ectromelia virus [1]. When CMX001 was administered orally to mice infected with HSV-1, mortality was reduced significantly (p≤0.001) with all three dose levels when treatments were initiated 24 h post viral inoculation. When treatments were started 48 h post viral inoculation, 5 and 2.5 mg/kg significantly reduced mortality (p≤ 0.001). If treatments were delayed until 72 h post viral inoculation, CMX001 did not reduce mortality or increase the mean day to death. When mice were infected intranasally with HSV-1 and treatments initiated 24 h post viral inoculation using CMX001 at 5 mg/kg or ACV at 100 mg/kg, virus replication in target organs was reduced by both CMX001 and ACV when compared to vehicle treated mice [2]. Toxicity: Diarrhea was the most common adverse event in patients receiving CMX001 at doses of 200 mg weekly or higher and was dose-limiting at 200 mg twice weekly. Myelosuppression and nephrotoxicity were not observed [4].

CNDAC is the active component of sapacitabine.

CNV1014802(GSK-1014802) is a novel small molecule state-dependent sodium channel blocker; Nav1.7 sodium channel inhibitor.

CO-1686 hydrobromide is a novel, irreversible and orally delivered kinase inhibitor that specifically targets the mutant forms of EGFR including T790M (IC50=21 nM).

CO-1686 is a novel, irreversible and orally delivered kinase inhibitor that specifically targets the mutant forms of EGFR including T790M(IC50=21 nM).

Cobicistat (GS-9350) is a potent and selective inhibitor of CYP3A with IC50 of 30-285 nM.

Coblopasvir (KW136, KW-136) is a novel HCV NS5A inhibitor under development for treatment of HCV infection..

Conivaptan(YM 087) is a non-peptide inhibitor of antidiuretic hormone (vasopressin receptor antagonist) with Ki values of 0.48 and 3.04 nM for rat liver V1A receptor and rat kidney V2 receptor respectively.

COTI-2 is a small molecule candidate anti-cancer drug which can convert mutant p53 to wild-type conformation.

CP-547632 is as a potent inhibitor of the VEGFR-2 and basic fibroblast growth factor (FGF) kinases (IC50 11 and 9 nM, respectively).

CPHPC(GSK2315698,Miridesap) is a divalent crosslinker of SAP that causes rapid depletion of circulating SAP via hepatic clearance.

CPI-444 is an orally administered antagonist of the adenosine A2A receptor. It is designed to block the action of adenosine that is produced by tumors.

CR6086 (CR-6086) is a potent, selective prostaglandin E2 receptor 4 (EP4) antagonist with Ki of 16.6 nM (hEP4 receptor), inhibits PGE2-stimulated cAMP production with IC50 of 22 nM.

Crenolanib (CP-868596) is a potent and selective inhibitor of PDGFRα/β with Kd of 2.1 nM/3.2 nM, also potently inhibits FLT3, sensitive to D842V mutation not V561D mutation, >100-fold more selective for PDGFR than c-Kit, VEGFR-2, TIE-2, FGFR-2, EGFR, erbB

Cridanimod sodium is a potent type I interferon (IFN) inducer that directly binds to STING and triggers a strong antiviral response through the TBK1/IRF3 route.

Cromolyn sodium is an antiallergic drug.

CTS-1027 is a potent small molecule inhibitor of MMPs(IC50=0.4 nM/0.6 nM for MMP2/MMP13); >1,000 fold selectivity over MMP1.

CUDC-101 is a potent multi-targeted inhibitor against HDAC, EGFR and HER2 with IC50 of 4.4 nM, 2.4 nM, and 15.7 nM, and inhibits class I/II HDACs, but not class III, Sir-type HDACs. Phase 1.

CVT-10216 is a potent and selective, reversible inhibitor of aldehyde dehydrogenase 2 (ALDH2) (IC50 values are 29 and 1300 nM for ALDH2 and ALDH1, respectively).

CWHM-12 a novel small molecule inhibitor of αV integrins with IC50s of 1.8/0.8/1.5/0.2 nM for αvβ1/αvβ3/αvβ8; less potency on αvβ5(IC50=61 nM) and on inhibition on αIIbβ3/α2β1/α10β1.

CX-4945 (Silmitasertib) is a potent and selective ATP-competitive small molecule protein kinase CK2 inhibitor with a Ki and an IC50 of 0.38 and 1 nM for recombinant human CK2α, respectively.

CX-5461 is an inhibitor of rRNA synthesis, selectively inhibits Pol I-driven transcription of rRNA, has no effect on Pol II, and possesses 250-to 300-fold selectivity for inhibition of rRNA transcription versus DNA replication and protein translation.