Metuzumab
Metuzumab (Licartin) is a human-mouse chimeric IgG1 monoclonal antibody targeting CD147. Metuzumab induces Apoptosis, reduces levels of Cyclin D1, full-length Caspase-3, and Bcl-2, and increases Bax expression. Metuzumab enhances the sensitivity of non-small cell lung cancer (NSCLC) cells to Gemcitabine (HY-17026). Metuzumab is applicable for research on hepatocellular carcinoma and non-small cell lung cancer [1] [2].
For research use only. We do not sell to patients.
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Caspase Isoforms
More
Biological Activity
Description
Species Reactivity
Human
IC50 & Target
|
Caspase-3 |
Bcl-2 |
Bax |
In Vitro
Metuzumab (0.1-100 μg/ml; 48 h) inhibits migration of SMMC-7721 cells in 2D culture in a dose-dependent manner[1].
Metuzumab (0.1-100 μg/ml; 24 h) inhibits invasion of SMMC-7721 cells in 2D Transwell assays in a dose-dependent manner[1].
Metuzumab (0.1-100 μg/ml; 48 h) inhibits proliferation of SMMC-7721 cells in 2D, 3DP, and 3DPF models in a dose-dependent manner[1].
Metuzumab (24 h) induces G1-phase arrest in A549, NCI-H460, and NCI-H520 NSCLC cells when combined with Gemcitabine, downregulating cyclin D1[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:human hepatocellular carcinoma SMMC-7721 cells (2D model)
-
Concentration:0.1-100 μg/ml
-
Incubation Time:48 h
-
Result:Decreased migration distance with increasing dose; distances for 1, 10, 100 μg/ml groups were 126.1 ± 6.7 μm, 98.8 ± 2.4 μm, 73.3 ± 8.5 μm, respectively, all significantly shorter than negative control and 0.1 μg/ml groups
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:BALB/c athymic nude mice (female, 5–6 weeks old)[2]
-
Dosage:10 mg/kg
-
Administration:twice weekly
-
Result:Reduced tumor volume by 39.34% (A549), 36.39% (NCI-H460), and 35.18% (NCI-H520) compared to saline controls. Enhanced tumor growth inhibition to 91.89% (A549, p < 0.001 vs. GP alone), 73.99% (NCI-H460, p = 0.0001 vs. GP alone), and 69.74% (NCI-H520, p < 0.001 vs. GP alone) when combined with GP. Increased deoxycytidine kinase (dCK) expression by 2.1-fold (A549), 1.4-fold (NCI-H460), and 1.7-fold (NCI-H520) in tumor tissues (measured by IOD).
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
-
Product Image
Application
ELISA, FACS, Functional assay
Chemical Information
-
Synonyms
Licartin; Metuximab; Mehuzumab
-
Formulation
Please refer to the lot-specific COA for specific buffer information.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
-
Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
-
TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
-
Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
-
Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
-
Liver Cancer Modeling
Liver cancer can be classified into primary liver cancer and secondary liver cancer. Secondary liver cancer is the metastatic liver cancer. Primary liver cancer includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and fibrolamellar HCC, of which HCC is the most common form, accounting for approximately 90% of primary liver cancers[1]. HCC mouse models include chemical agent-induced models, transplanted tumor models, and genetic engineered models.
Purity & Documentation
References
[1]. Li Y, et al. 3D bioprinting of hepatoma cells and application with microfluidics for pharmacodynamic test of Metuzumab. Biofabrication. 2019;11(3):034102. Published 2019 Jun 26. [Content Brief]
[2]. Feng F, et al. Metuzumab enhanced chemosensitivity and apoptosis in non-small cell lung carcinoma. Cancer Biol Ther. 2017;18(1):51-62. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Metuzumab
- Licartin
- Metuximab
- Mehuzumab
- Apoptosis
- CDK
- Caspase
- Bcl-2 Family
- apoptosis
- Bcl-2
- full-length caspase-3
- A549
- antibody-dependent cell-mediated cytotoxicity
- non-small cell lung carcinoma
- SMMC-7721 cells
- NCI-H520
- Bax
- deoxycytidine kinase
- NSCLC xenograft models
- cisplatin
- cyclin D1
- gemcitabine
- 3D co-culture microfluidic models
- NCI-H460
- BALB/c athymic nude mice
- G1 arrest
- CD147
- PBMCs
- hepatoma cells
- Inhibitor
- inhibitor
- inhibit