Catalog #SIM0051
InVivoSIM anti-human TROP-2 (Sacituzumab Biosimilar)
Clone
Sacituzumab
Reactivities
Human
Product Citations
1
Isotype
Human IgG1, κ
Product Description
This biosimilar antibody uses the same variable regions as the therapeutic antibody Sacituzumab, making it ideal for research use. Sacituzumab is a fully humanized IgG1κ monoclonal antibody that reacts with human trophoblastic cell surface antigen 2 (TROP-2), an antigen linked to cancer. TROP-2 is a cell surface receptor that spans the cellular membrane with an extracellular, transmembrane, and intracellular domain, along with a cytoplasmic tail essential for signaling. The ligands of TROP-2 include claudin-1, claudin-7, cyclin D1, and potentially IGF-1. TROP-2 upregulates EpCAM-triggered cell signaling and requires RIP to regulate efficient growth and division of cancer cells. Several proteins, including RIP, TACE, γ-secretase, Presenilin 1 (PS-1) and PS-2, facilitate TROP-2’s cleavage within the transmembrane domain, and this cleavage produces TROP-2 extracellular domain (ECD) and intracellular domain (ICD) fragments. TROP-2 is considered a cellular marker of trophoblastic stem cells, and this glycoprotein is known to transduce calcium signals. Normal epithelial cells express TROP-2 at a low level, while many tumors (such as glioblastoma, pancreatic carcinoma, and all breast cancer subtypes, especially triple-negative breast cancer) express it at a high level. The critical role of TROP-2 in multiple signaling pathways often links to the proliferation, invasion, and metastasis of tumors. The tumor cell-specific expression of TROP-2 makes it an ideal target for cancer immunotherapy. Several recent studies have used Sacituzumab-based antibody-drug conjugates (ADC), namely Sacituzumab Govitecan (IMMU-132) that contains Sacituzumab conjugated to SN-38 (the active metabolite of irinotecan), utilizing a pH hydrolysable linker CL2A for facilitating SN-38 release to the cancer cells in in vitro and in vivo preclinical studies.
Specifications
| Isotype | Human IgG1, κ |
|---|---|
| Recommended Isotype Control(s) | RecombiMAb human IgG1 (K214R/L234F/L235E/P331S) isotype control, anti-hen egg lysozyme |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Mutations | K214R |
| Immunogen | Human TROP-2 |
| Reported Applications |
in vitro functional assays in vivo functional assays Antibody-drug conjugate synthesis ELISA Western blot Flow cytometry |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
≤0.5EU/mg (≤0.0005EU/μg) Determined by LAL assay |
| Aggregation |
<5% Determined by SEC |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Molecular Weight | 150 kDa |
| Murine Pathogen Tests |
Ectromelia/Mousepox Virus: Negative Hantavirus: Negative K Virus: Negative Lactate Dehydrogenase-Elevating Virus: Negative Lymphocytic Choriomeningitis virus: Negative Mouse Adenovirus: Negative Mouse Cytomegalovirus: Negative Mouse Hepatitis Virus: Negative Mouse Minute Virus: Negative Mouse Norovirus: Negative Mouse Parvovirus: Negative Mouse Rotavirus: Negative Mycoplasma Pulmonis: Negative Pneumonia Virus of Mice: Negative Polyoma Virus: Negative Reovirus Screen: Negative Sendai Virus: Negative Theiler’s Murine Encephalomyelitis: Negative |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Product Citations
-
Payload Diversification Overcomes Resistance and Guides Sequential Antibody-Drug Conjugate Therapy in Breast Cancer.
In Clin Cancer Res on 15 April 2026 by Rampa, D. R., Seo, M., et al.
PubMed
Antibody-drug conjugates (ADC) have transformed the treatment of breast cancer. FDA-approved ADC such as trastuzumab deruxtecan (T-DXd), sacituzumab govitecan (SG), and datopotamab deruxtecan (Dato-DXd) have demonstrated clinical benefit; however, drug resistance will almost inevitably emerge in the metastatic setting, and there is no established strategy for selecting subsequent ADC after disease progression following the first exposure to the ADC. This study aimed to define mechanisms of acquired resistance and evaluate rational sequencing approaches.