cbl

Cbl-b-IN-3 is a potent inhibitor of casitas b lineage lymphoma proto-oncogene-b (Cbl-b) (ic50 < 1 nM).

Cbl-b-IN-5 is a potent CPL-B inhibitor with IC50 values between 3 and 10 µM. Cbl-b-IN-5 has been used to study cancer and diseases related to the immune system.

hydrocotarnine is an inhibitor of Cbl.

PROTAC Cbl-b-IN-1 is a PROTAC that targets Cbl-b. It is composed of the PROTAC targeting protein ligand Cbl-b-IN-21, PROTAC Linker Cbz-Pip-2C-Pip-C-Pip, and the E3 ubiquitin ligase ligand (3S)Lenalidomide-5-Br. The conjugate of the E3 ubiquitin ligase ligand and Linker is (3S)Lenalidomide-5-Pip-C-Pip-2C-Pip.

Cbl-b-IN-26 (Example A1) is an inhibitor of Cbl-b with a dissociation constant (Kd) of 34.6 nM. It is used in the research of chronic viral infections and cancer.

Cbl-b-IN-1 is a potent Cbl-b inhibitor (IC50 <100 nM) with potential anticancer activity for the study of intestinal inflammation.

Cbl-b-IN-2 is an orally active biological compound that inhibits the E3 enzyme Casitas b lineage lymphoma proto-oncogene b (Cbl-b) in the ubiquitin proteasome pathway and can be used in the study of diseases that modulate the immune system and are susceptible to regulation by the immune system. Cbl-b-IN-2 can also be used in cancer research alone or in combination with one or more immune checkpoint inhibitors, antitumour agents and radiopharmaceuticals.

Cbl-b-IN-6 (Compound 246) is an inhibitor of casitas B-lineage lymphoma-b (Cbl-b) and c-Cbl, with half-maximal inhibitory concentrations (IC50s) of 6.7 nM for Cbl-b and 5.2 nM for c-Cbl, respectively [1].

Cbl-b-IN-7 (Compound 248) is an inhibitor of casitas B-lineage lymphoma-b (Cbl-b) and c-Cbl, with half-maximal inhibitory concentrations (IC50s) of 6.7 nM and 5.2 nM, respectively [1].

Cbl-b-IN-8 (Compound 293) is an inhibitor of casitas B-lineage lymphoma-b (Cbl-b) and c-Cbl, with half maximal inhibitory concentrations (IC50s) of 5.5 nM and 7.8 nM, respectively [1].

Cbl-b-IN-9 (Compound 300) is a potent inhibitor targeting casitas B-lineage lymphoma-b (Cbl-b) and c-Cbl, with half-maximal inhibitory concentrations (IC50s) of 5.6 nM and 4.7 nM, respectively [1].

Cbl-b-IN-10 (Compound 463) is a potent inhibitor of both casitas B-lineage lymphoma-b (Cbl-b) and c-Cbl, with half-maximal inhibitory concentrations (IC50s) of 6.0 nM and 3.5 nM, respectively [1].

Cbl-b-IN-11 (Compound 466) is an inhibitor of casitas B-lineage lymphoma-b (Cbl-b) and c-Cbl, with half-maximal inhibitory concentrations (IC50s) of 6.4 nM and 6.1 nM, respectively [1].

Cbl-b-IN-12 (Example 10) is a CBL-B inhibitor with an IC50 of less than 100 nM [1].

Cbl-b-IN-13 (Example 520) is a potent Cbl-b inhibitor with an IC50 of less than 100 nM, capable of activating T-cells [1].

Cbl-b-IN-27 is an inhibitor of the B lymphoma proto-oncogene b (Cbl-b), with an IC50 value of 7 nM. This compound is promising for research into the regulation of effector T cell function, T cells, natural killer (NK) cells, and B cell activation.

Cbl-b-IN-21, a PROTAC target protein ligand (Ligands for Target Protein for PROTACs), serves as a key component in the synthesis process.

CBL0137 hydrochloride (Curaxin-137 hydrochloride) is an inhibitor of the histone chaperone FACT, which also activates p53 and inhibits NF-κB with EC50 values ​​of 0.37 and 0.47 μM, respectively. CBL0137 hydrochloride functionally inactivates the complex that promotes chromatin transcription (FACT), thereby driving effects on p53 and NF-κB and promoting cancer cell death, and when used in combination with cisplatin, CBL0137 hydrochloride has potent anticancer activity against SCLC.

CBL0137 (Curaxin 137), a metabolically stable curaxin, activates p53 (EC50: 0.37 μM) and inhibits NF-κB (EC50: 0.47 μM). It functionally inactivates the facilitates chromatin transcription complex (FACT), driving the effects on p53 and NF-κB and promoting cancer cell death. CBL0137 has broad anticancer activity in mice when administered orally, eradicates drug-resistant cancer stem cells, and potentiates the efficacy of gemcitabine in preClinicalal models of pancreatic cancer.

CBL0100 is an inhibitor of viral transcriptional elongation, blocking both HIV-1 replication and reactivation.

CBLB 612 is both an auxiliary anti-radiation and an anti-tumor agent [1].

(3S)Lenalidomide-5-Pip-C-Pip-2C-Pip serves as an E3 Ligase Ligand-Linker Conjugate and is utilized in the synthesis of PROTAC Cbl-b-IN-1.

Siamycin I is a tricyclic peptide originally isolated from Streptomyces and has antiviral and antibacterial activities. It is active against laboratory strains and clinical isolates of HIV-1 (ED50s = 0.05-0.45 and 0.89-5.7 μM, respectively), as well as the CBL-20 strain of HIV-2 (ED50 = 0.45 μM), in vitro. Siamycin I inhibits HIV-induced fusion of C8166 T cells with HIV-1-infected CEM-SS cells with an ED50 value of 0.08 μM. It is also active against B. subtilis, M. luteus, and S. aureus (MICs = 1.6-6.3 μg/ml). Siamycin I inhibits autophosphorylation of the E. faecalis quorum sensing kinase FsrC induced by gelatinase biosynthesis-activating pheromone (GBAP).

Arsthinol is an antiprotozoal agent which may have anti-cancer activity. It was found that arsthinol, a trivalent organoarsenic compound (dithiarsolane), has been active in vitro on leukemia cell lines and offers a better therapeutic index than arsenic trioxide, as estimated by the ratio LD50 IC50. Arsthinol induced growth inhibition of NB4 cells at lower concentration (IC50 (concentration inhibiting growth by 50%) = 0.78 + - 0.08 micromol l after 24 h) than As(2)O(3) (IC50 = 1.60 + - 0.23 micromol l after 24 h) or melarsoprol (IC50 = 1.44 + - 0.08 micromol l after 24 h). Arsthinol-cyclodextrin complex demonstrated to have was more effective than arsenic trioxide (As2O3) and melarsoprol on the U87 MG cell line. Importantly, in the in vivo study, significant antitumor activity against heterotopic xenografts was observed after i.p. administration.