Cycloheximide (Naramycin A, Actidione) is a widely-used protein synthesis inhibitor that inhibits protein biosynthesis in eukaryotic organisms with IC50 of 532.5 nM and 2880 nM for protein synthesis and RNA synthesis in vivo, respectively; block the elongation phase of eukaryotic translation, binds the ribosome and inhibits eEF2-mediated translocation; impairs memory more as footshock intensity increases, enhances memory in an inverted-U dose-response manner at low dose; also sensitizes COLO 205 cells to TNF-alpha-induced programmed cell death.

CXF-009 is a potent, specific, dual-warhead covalent inhibitor of FGFR4 (IC50=48 nM), forms dual-warhead covalent bonds with two cysteine residues in FGFR4.CXF-009 forms covalent bonds with FGFR4(C477A) and FGFR4(C552A), respectively; display weak inhibition against FGFR1-3 with IC50 of 2579 nM, 2408 nM, and 977 nM.CXF-009 shows inhibitory effect agaginst FGFR4 muntants FGFR4(C477A), FGFR4(C552A), and FGFR4(C477A, C552A) with IC50 of 193 nM, 602 nM, and 1528 nM, respectively.CXF-009 inhibited the growth of Ba/F3 cells transformed with FGFR1-4 with IC50 values of 1562 nM, 1971 nM, 777 nM, and 38 nM, respectively.CXF-009 is slightly more reactive to GSH than PRN1371.

CXCR7 modulator 20 is a small molecule modulator of the atypical chemokine receptor CXCR7 with Ki of 52 nM.

CU7218 is a small-molecule inhibitor of 14-3-3 protein, inhibits the interaction between 9J10 and 14-3-3, displaces FOXO3a and other substrate proteins from 14-3-3 and reproduces the cellular phenotypes induced by 9J10 expression.

CU-72 is a potent, selective TLR7/8 dual inhibitor with IC50 of 5.10 and 2.87 uM, respectively.

C-type natriuretic peptide (CNP, pGC-B activator) is the native particulate guanylyl cyclase B receptor (pGC-B) activator.CNP induces anti-remodeling actions in the heart and kidney through the generation of the second messenger cGMP.CNP selectively activates pGC-B and generates cGMP in vitro.CNP is abundantly expressed in the endothelium and kidneys as well as the heart, but to lesser extent than trial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP).CNP is produced as a prohormone that is cleaved intracellularly by the enzyme, furin, to yield a 53-AA intermediate form (C53).

CTN1122 (CTN-1122) is a potent, selective Leishmaniacasein kinase 1 isoform 2 (CK1.2, L-CK1.2) with IC50 of 0.72 uM (LmCK1) and 0.8 uM (amastigotes L. major), antileishmanial compound.

CTCB-405 (CTCB405) is a small molecule allosteric inhibitor of T. brucei phosphofructokinase (TbPFK) with IC50 of 0.18 uM, ITC Kd of 92 nM, no significant inhibition of human PFKs.CTCB-405 demonstrated in vitro parasite killing potency of the bloodstream form of T. brucei strain Lister 427 (EC50=0.37 uM).CTCB-405 (50, 100 mg/kg) clear parasites in a stage 1 model of HAT infection with 1-day oral dosing and show reduction of parasitaemia in the brain in a pleiomorphic model.

CS640 (CS-640) is a potent, selective CaMK1D inhibitor with nanomolar range at both the enzymatic and cellular levels.CS640 prevent Aβ induced tau hyperphosphorylation in culture, but were not able to protect cells from Aβ induced toxicity.CS640 was able to ablate Aβ induced increased tau phosphorylation at Thr181 in mouse primary neurons.

CRL inhibitor 33-11 is a small moelcule E3 CRL inhibitor, directly and selectively binds to the purified E3 ROC1-CUL4A CTD and ROC1-CUL1 CTD complex with Kd of 0.223 and 4.53 uM, respecitvely.CRL inhibitor 33-11 binds to ROC1-CUL1 more effectively than ROC1-CUL1-Nedd8.CRL inhibitor 33-11 showed the ability to inhibit ubiquitination by ROC1–CUL1 more potently than that by ROC1-CUL1-Nedd8.CRL inhibitor 33-11 inhibited the ubiquitination of CK1α by CRL4CRBN in vitro.

CRCM5484 is a potent, BET BDII-selective inhibitor with IC50 of 130/20/71 nM for BRD4-BD2/BRD3-BD2/BRD2-BD2, respectively.CRCM5484 displays 475-fold selectivity over its first bromodomain (BRD3-BD2 vs BRD3-BD1).CRCM5484 demonstrates very low activity in various cell-based assays.CRCM5484 modulates the anti-leukemic activity in combination with various FDA-approved and/or in-development drugs in a cell- and context-dependent differential manner.

CPL500036 (CPL-500036) is a highly potent, selective and orally bioavailable PDE10A inhibitor with IC50 of 35 nM.CPL500036 is highly selective for PDE10A over other PDEs and common off-targets.CPL500036 effectively penetrates the brain where increases cAMP/cGMP levels and phosphorylates effector proteins like AMPA subunits.CPL500036 reduced sensorimotor deficits in 6-OHDA-lesioned rats.Acute and chronic CPL500036 did not reduce effects of L-DOPA in sensorimotor tests.Chronic CPL500036 treatment did not decrease L-DOPA-induced contralateral rotation.

CPL302-253 is a potent, selective inhibitor of PI3Kδ with IC50 of 12.2 nM and Kd of 0.83 nM, >350-fold selectivity over PI3K isoforms α, β, and γ (IC50>4,500 nM); CPL302-253 displays no off-target interaction in KinomeScan assays. CLP302-253 blocks activation of primary lymphoid cells in vitro, blocks IL-33 cytokine production in epithelial and T cell co-cultures. CLP302-253 bocks eosinophil infiltration to the lungs and IL-33 expression in HDM induced asthma mouse model.

Cotadutide (MEDI-0382) is a dual GLP-1/glucagon receptor peptide agonist with robust anti-obesity and metabolic effects.

COR588 is a second-generation small-molecule lysine-gingipain (Kgp, gingipain K) inhibitor with novel structure and improved pharmacologic and safety profile prioritized for Alzheimer’s development.

COR388 (Atuzaginstat) is an orally bioavailable, brain penetrant small-molecule that irreversibly inhibits lysine-gingipain (Kgp, gingipain K) with Ki of <0.01 nM.COR388 blocks the activity of gingipains, a type of toxic protein made by the bacteria Porphyromonas gingivalis ( P. gingivalis ).COR388 reduced the bacterial load of an established P. gingivalis brain infection, blocked Aβ1-42 production, reduced neuroinflammation, and rescued neurons in the hippocampus.

Cobalt protoporphyrin IX (CoPPIX) is a potent and effective inducer of HO-1 (heme oxygenase-1) activity, up-regulates HO-1 via Bach1 and Nrf2 in human liver cells.CoPPIX did not influence hepatic Bach1 or Nrf2 mRNA levels, but markedly reduced Bach1 protein levels by increasing degradation of Bach1 protein, and increased Nrf2 by decreasing degradation of Nrf2 protein.CoPPIX significantly upregulated HO-1 protein in mucosal and submucosal cells.CoPPIX is a direct Bach1 inhibitor.

COB-187 (COB187) is a highly potent and selective inhibitor of GSK-3 with IC50 of 22/11 nM against GSK-3α/GSK-3β.COB-187 inhibits GSK-3 phosphorylation of β-catenin and, albeit to a lesser extent, glycogen synthase.COB-187 increases the protein level of β-catenin in RAW 264.7 macrophages.COB-187 enhances β-catenin localization to the perinuclear and nuclear region in THP-1 macrophage, does not change the β-catenin mRNA level.COB-187 significantly increases the expression of the Wnt target gene cyclin D1, reduces the phosphorylation of tau in HEK293 cells transfected with tau expression vector.COB-187 inhibits only 3 kinases at >40% in a panel of 414 kinase assays, more selective relative to Tideglusib.

CNBDA is a novel selective Src homology phosphotyrosine phosphatase 2 (SHP2) inhibitor with IC50 of 5 uM, 25-fold selectivity over SHP1.Treatment HER2-positive BC cells with CNBDA suppressed cell proliferation in 2D culture, anchorage-independent growth in soft agar, and mammosphere (tumorisphere) formation in suspension cultures in a concentration-dependent manner.CNBDA inhibited EGF-induced signaling and expression of HER2 by inhibiting the PTPase activity of SHP2 in BC cells.

Cl-OCH3 is an antagonist of nuclear receptor NR4A1, decreases PD-L1 protein expression in MDA-MB-231 and 4T1 cells with EC50 of 4.4 and 4.1 uM, respectively; Cl-OCH3 decreased expression of PD-L1 mRNA, promoter-dependent luciferase activity, and protein. In in vivo studies using a syngeneic mouse model bearing orthotopically injected 4T1 cells, Cl-OCH3 decreased tumor growth and weight and inhibited lung metastasis. Cl-OCH3 also decreased expression of CD3+/CD4+/CD25+/FoxP3+ regulatory T cells and increased the Teff/Treg ratio.

CLK4 inhibitor 96 is a novel potent CLK4 inhibitor with IC50 of 57.5 nM.

CK2 inhibitor KN2 is a potent, highly selective, cell-permeable, bivalent CK2 inhibitor, binds to CK2α- and CK2α′-based CK2 holoenzymes with Ki of 6.1 nM (CK2α2β2) and 4.0 nM (CK2α′2β2).KN2 inhibits CK2α- and CK2α′-based CK2 holoenzymes with IC50 of 19.3 nM (CK2α2β2) and 15.6 nM (CK2α′2β2) at 100 uM ATP.KN2 downregulated the CK2-dependent phosphorylation level of Akt phosphorylation at Ser129 (p-Akt S129).

CJ-1639 (CJ1639) is a potent, highly selective dopamine D3 receptor (D3R) full agonist with Ki of 0.5 nM, >5,000-fold selectivity over D1 and D2 receptors in binding assays.CJ-1639 binds to human D3 receptor with a K(i) value of 3.61 nM and displays over >1000-fold selectivity over human D1 and D2 receptors.CJ-1639 is an excellent pharmacological tool to elucidate the role of the D3 receptor in different neurological conditions in animal models.

CIGB-300 (P15-Tat) is a cell-permeable cyclic peptide that modulates CK2 (CSNK2) activity by binding to the phosphoacceptor site on CK2 targets, abrogates the CK2 phosphorylation by blocking recombinant substrates in vitro.CIGB-300 (P15-Tat) induced apoptosis as evidenced by rapid caspase activation and cellular cytotoxicity in a variety of tumor cell lines (HSCLC H-82 cell IC50=20 uM).CIGB-300 (P15-Tat) demonstrated substantial regression of the tumor mass C57BL6 mice bearing day 7-established solid tumors.CIGB-300 (P15-Tat) reduced breast cancer cell growth in MDA-MB-231, MCF-7 and F3II cells, exerting a pro-apoptotic action and cell cycle arrest. CIGB-300 decreased cell adhesion, migration and clonogenic capacity of malignant cells.CIGB-300 may interfere with the SARS-CoV-2 life cycle within infected human cells.

Ciapavir (SBI-0953294, cIAP1 antagonist for viral reactivation) is a bivalent, next-generation, Smac mimetic and antagonist of cIAP1 as latency-reversing agent (LRA), specifically and potently promote HIV-1 latency reversal activity both in vivo.Ciapavir's latency reversal activity is dependent on the NIK-dependent NF-κB signaling.Ciapavir exhibits substantially greater potency and efficacy as an LRA, inducing comparable levels of latency reversal at concentrations 10- to 1,000-fold lower than the first-generation molecule SBI-0637142, without an increase in cytotoxicity.Ciapavir does not trigger cytokine release or T cell activation.Ciapavir is capable of increasing latent HIV-1 expression in ART-treated BLT mice in vivo and may therefore prove useful in "shock and kill" approaches to HIV-1 cure.

CGX1321 (CGX-1321) is a nove potent and specific inhibitor of porcupine (PORCN) that inhibits Wnt pathway, block secretion of WNT proteins with IC50 of 1 nM; CGX1321 displayed >500 times selective for Porcupine over the most related target enzyme, hedgehog acyltransferase. CGX1321 increased Ki67+ and phosphohistone H3 (PH3+) cardiomyocytes in culture, up-regulated cell cycle regulating genes such as Ccnb1 and Ccne1, did not alter YAP protein phosphorylation and nuclear translocation in cardiomyocytes. CGX1321 administration blocked the secretion of Wnt proteins, and inhibited both canonical and non-canonical Wnt signaling pathways in MI injury mice. CGX1321 improved cardiac function, reduced myocardial infarct size, and fibrosis of post-MI hearts. CGX1321 significantly increased newly formed cardiomyocytes in infarct border zone of post-MI hearts, evidenced by the increased EdU+ cardiomyocytes.

CFT-14441 is a potent and selective BRD9 BiDAC degrader with DC50 of 39 nM (2h), high selectivity over BRD4 abd BRD7.CFT-14441 efficiently degrades endogenous BRD9 in the Yamato-SS synovial sarcoma cell line, results in growth inhibition of BAF-perturbed HSSYII synovial sarcoma cells but not BAF-wild type SW982 soft tissue sarcoma cells.CFT-14441 demonstrates efficacy in both cell-derived and patient-derived models of synovial sarcoma (IV or IP dosing).

CFI-400945 is a potent, highly selective, orally available PLK4 inhibitor with Ki of 0.26 nM and IC50 of 2.8 nM, does not significantly inhibits PLK1/2/3 at 50 uM; causes dysregulated centriole duplication, mitotic defects, and cell death in multiple cancer cell lines (A549 GI50=5 nM, OVCAR-3 GI50=18 nM); significantly inhibits human cancer xenografts; causes polyploidy, growth inhibition, and apoptotic death of murine and human lung cancer cells, despite expression of mutated KRAS or p53, produces supernumerary centrosomes and mitotic defects in lung cancer cells.

CDDD2-94 is a highly potent and selective CDK4 inhibitor with Ki of 2 nM, >140-fold selective for CDK4 over CDK6 (Ki=279 nM).CDDD2-94 is ineffective against other members of the CDK family, displays high selectivity against a panel of 369 human kinases at 1uM, with exceptionally selective-CLK, DYRKs and MYLK4 were the only kinases targeted potently.CDDD2-94 is the most selective CDK4 inhibitor identified to date.CDDD2-94 demonstrated antiproliferative activityagainst MV4-11 and MDA-MB-453 cell lines with GI50 of 0.107 and 0.325 uM respectively.CDDD2-94 inhibits S780-phosphorylated Rb (pRb(S780)) and decreases transcription of Rb1 and E2F-target genes in MDA-MB-453 cells.CDDD2-94 is well tolerated and efficacious in preclinical OC xenograft model, CDDD2-94 provides better safety profile than palbociclib towards the bone marrow.

CDD-1102 (CDD1102) is a potent, selective second bromodomain (BD2) of BRDT and BRD4 inhibitor with IC50 of 7 and 25 nM, >1,000-fold and 300-fold selectivity over BRDT-BD1 and BRD4-BD1.