Cbl-b-IN-30
Cbl-b-IN-30 is an orally active Casitas B-lineage lymphoma-b (CBLB) inhibitor. Cbl-b-IN-30 specifically binds to CBLB and inhibits its E3 ubiquitin ligase activity with an IC50 of 9.1 nM. Cbl-b-IN-30 can promote IL-2 secretion (EC50 = 187.5 nM) and enhance T cell activation. Cbl-b-IN-30 exerts antitumor activity and can induce immune memory. Cbl-b-IN-30 can be used for the research of colon cancer.
For research use only. We do not sell to patients.
- Formula: C29H32F3N7O
- Molecular Weight:551.61
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
IL-2 |
In Vitro
Cbl-b-IN-30 (Compound 10) promotes IL-2 secretion (EC50 = 187.5 nM) and enhances T cell activation in human T cells activated by anti-CD3 antibody[1].
Cbl-b-IN-30 specifically binds to CBLB and inhibits its E3 ubiquitin ligase activity with an IC50 of 9.1 nM[1].
Cbl-b-IN-30 does not significantly inhibit CYP1A2/2C9/2C19/2D6/3A4 (IC50 >50 μM) and shows IC50 >30 μM for hERG, showing low risks of drug-drug interactions and cardiac toxicity[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
| Species | Dose | Route | Note | CL | AUC0-t | Cmax | T1/2 | F |
|---|---|---|---|---|---|---|---|---|
| Rat | 10 mg/kg | p.o. | 文献审核 | / | 1074.6 ng·h/mL | 260.9 ng/mL | 2.4 h | 29.1 % |
| Mice | 30 mg/kg | p.o. | 文献审核 | / | 3536.1 ng·h/mL | 2125.7 ng/mL | 4.3 h | 52.2 % |
| Dog | 5 mg/kg | p.o. | 文献审核 | / | 159.6 ng·h/mL | 114.4 ng/mL | 1.5 h | 8.4 % |
| Rat | 1 mg/kg | i.v. | 文献审核 | 44.7 mL/min/kg | / | / | / | / |
| Mice | 1 mg/kg | i.v. | 文献审核 | 74.4 mL/min/kg | / | / | / | / |
| Dog | 1 mg/kg | i.v. | 文献审核 | 44.3 mL/min/kg | / | / | / | / |
In Vivo
Cbl-b-IN-30 (30 mg/kg, p.o., daily for 15 days) combined with anti-PD-1 antibody induces durable immune memory in BALB/c mice with complete tumor response, showing no tumor growth after CT26 cell rechallenge with a survival rate of 100%[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:BALB/c mice bearing CT26 syngeneic tumors[1]
-
Dosage:3, 10 and 30 mg/kg
-
Administration:Orally administration
-
Result:Showed a TGI of 50% at 10 mg/kg without significant body weight loss.
Showed a TGI of 50% at 10 mg/kg companied with anti-PD-1 antibody.
Chemical Information
-
Molecular Weight 551.61
-
Formula C29H32F3N7O
-
SMILES
C[C@@H]1C[C@@](C2=NN=CN2C)(C3=CC=NC(N4C=NC(C(C(F)(F)F)=CC(CN5CCC[C@@H](C5)C)=C6)=C6C4=O)=C3)C1
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
-
Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
-
Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Cbl-b-IN-30
- E1/E2/E3 Enzyme
- Interleukin Related
- ADME properties
- pharmacokinetic profiles
- CBLB inhibitor
- structure-activity relationship
- antitumor efficacy
- syngeneic mouse models
- immune memory
- Cbl-b
- CBLB
- anti-PD-1 therapy
- downstream biomarkers
- target engagement
- tumor regression
- SAR
- compound 10
- Inhibitor
- inhibitor
- inhibit