Anti-Mouse CD106 (VCAM-1) (Clone M/K-2.7) – Purified in vivo PLATINUM™ Functional Grade

Clone M/K-2.7 is a rat monoclonal antibody targeting mouse CD106 (VCAM-1), and its common in vivo applications in mice include:

• Neutralization of VCAM-1 activity in physiological and pathological studies, especially for investigating leukocyte adhesion, transmigration, and inflammation.
• Functional assays to study biological pathways affected by VCAM-1, including immune cell trafficking, inflammation, and tissue injury models.
• Disease models such as:
  • Collagen-induced arthritis, where M/K-2.7 is used to modulate joint inflammation by neutralizing VCAM-1.
  • Liver injury studies, where administration of M/K-2.7 exacerbated liver damage and apoptosis, suggesting its role in studying immune cell (e.g., NK cell) depletion and tissue injury mechanisms.
  • Cardiovascular research, particularly in hypertensive heart conditions and subretinal fibrosis, to investigate VCAM-1’s contribution to cardiovascular pathology.

Additional details:

• The antibody is frequently used for in vivo neutralization experiments, meaning it is administered to living mice to block VCAM-1 function and study immune, inflammatory, or vascular mechanisms.
• It is also applied in immunofluorescence and flow cytometry for labeling and tracking VCAM-1 expressing cells in tissues, though in vivo blockade is its primary research purpose.

In summary, clone M/K-2.7 is widely used for in vivo VCAM-1 neutralization to investigate immune cell adhesion, inflammatory disease mechanisms, and tissue injury in mouse models.

Commonly, when M/K-2.7 (a rat anti-mouse VCAM-1, or CD106, monoclonal antibody) is used in research, it is paired with antibodies and proteins that detect related cellular markers or components involved in leukocyte adhesion, vascular biology, and immune cell characterization.

Frequently co-used antibodies and proteins with M/K-2.7:

• CD31 (PECAM-1): Used to identify endothelial cells, often alongside VCAM-1 to analyze vascular endothelium integrity or inflammation.
• CD45: A pan-leukocyte marker, used to define infiltrating leukocytes versus endothelial or stromal cells.
• ICAM-1 (CD54): Another adhesion molecule, commonly measured in conjunction with VCAM-1 to assess endothelial activation or leukocyte transendothelial migration.
• CD49d (Integrin α4, part of VLA-4 complex): The ligand for VCAM-1, used to evaluate interactions between leukocytes and the endothelium.
• Ly6G (neutrophils), F4/80 (macrophages), CD3 (T cells): Immune subset markers to characterize the specific immune cell types adhering or transmigrating in VCAM-1–mediated processes.
• Isolectin B4 or Lectin GS-IB4: For detailed vascular endothelium labeling and to complement VCAM-1 staining in imaging.

Rationale for common combinations:
Research using M/K-2.7 frequently aims to study inflammation, immune cell trafficking, or vascular biology—contexts where cell adhesion and immune cell identity are central. Thus, VCAM-1 is most informative when analyzed together with markers of endothelial cells, leukocytes, other adhesion molecules, and ligands such as VLA-4.

Example applications in literature:

• Immunofluorescence or flow cytometry studies often incorporate anti-VCAM-1 (M/K-2.7) with anti-CD31 and anti-CD45 to clearly distinguish endothelial cells from immune infiltrates.
• Functional studies may block both VCAM-1 (with M/K-2.7) and ICAM-1 to dissect their respective roles in leukocyte adhesion and transmigration.
• In vivo depletion or blocking protocols combine M/K-2.7 with antibodies against specific immune cells (e.g., anti-NK1.1, anti-CD4) to interrogate cell–cell interactions in disease or injury models.

There are no single “standard” combinations, but pairings strongly reflect the immunological or vascular processes under study, with markers for endothelial cells (CD31), leukocytes (CD45), adhesion molecules (ICAM-1), and interacting integrins (CD49d/VLA-4) being most frequent.

The key findings from scientific literature citing clone M/K-2.7 focus on its use as a monoclonal antibody targeting mouse VCAM-1 (vascular cell adhesion molecule-1), with impactful roles in immunology and transplantation studies.

• M/K-2.7 specifically binds to mouse VCAM-1 (CD106): This antibody recognizes the Ig-like domains 1 and 4 of VCAM-1, making it a common reagent for mouse endothelial cell and inflammation studies.
• Functional blockade of VCAM-1: M/K-2.7 is frequently used to disrupt VCAM-1-mediated cellular adhesion and transendothelial migration, particularly in studies of immune cell trafficking and transplantation. Treatment with M/K-2.7 has been shown to inhibit leukocyte adherence and migration, and modulate inflammation.
• Impact on Transplant Survival and Rejection: In murine transplant models, M/K-2.7 prolongs islet and cardiac allograft survival and alleviates rejection, suggesting a key therapeutic potential for limiting immune-mediated damage post-transplantation. Allograft survival increases by more than 100 days in islet models and by five days in cardiac models following M/K-2.7 treatment.
• Research reagent characteristics: M/K-2.7 is a rat IgG1 κ monoclonal antibody, validated for flow cytometry, immunohistochemistry, and in vivo blockade in mouse models.

Additional relevant findings:

• In immunological assays: M/K-2.7 is used as a tool for detecting VCAM-1 protein expression in tissues and cell cultures, and is cited in protocols for assessing inflammatory signaling and vascular activation.
• Commercial availability: The clone is sold by major antibody suppliers for research use in mouse, with over 16 product citations indicating broad adoption in biomedical studies.

There are no conflicting results regarding the specificity or in vivo functional role of M/K-2.7, which supports its widespread use as the standard anti-mouse VCAM-1 reagent.

Dosing regimens for clone M/K-2.7 (anti-mouse CD106/VCAM-1) vary depending on the study design and mouse disease model, but published regimens commonly use intraperitoneal (i.p.) injection at doses ranging from 0.1 to 0.2 mg every two days for 14 days.

In cardiac dysfunction models, M/K-2.7 has been administered at 0.1 mg or 0.2 mg per mouse (i.p.) once every two days for a total of 14 days. This regimen was shown to dose-dependently improve cardiac function and reduce tissue damage.

In immunology and infection studies:

• M/K-2.7 has been used to modulate tissue-resident memory (TRM) CD4 T cell formation in the lung, though dosing specifics were not detailed in the summary provided.
• For natural killer (NK) cell depletion, M/K-2.7 has been used to enhance viral clearance; the dosing regimen in these models is typically aligned with those outlined for depletion studies (i.e., repeated dosing every few days, similar to other monoclonal depletion antibodies).

Route of Administration:
The antibody is generally administered intraperitoneally in mouse models, which matches practices for most in vivo monoclonal antibody studies.

Model-specific notes:

• In cardiac models, efficacy was shown for both 0.1 mg and 0.2 mg doses, indicating that dose selection may be guided by disease severity or experimental endpoint.
• In infection and immune cell modulation studies, the dosing often parallels protocols used for other immune cell depleting antibodies, typically in the range of 100–250 μg (0.1–0.25 mg) per mouse every 2–3 days.

Key points:

• Typical dose: 0.1–0.2 mg/mouse (i.p.) every two days for 14 days in cardiac and immunology models.
• Variation: Dose schedule may be adapted depending on disease kinetics, mouse strain, and whether acute or chronic intervention is intended.
• Other models: Some studies use similar antibodies with dosing regimens in the 100–250 μg/mouse range every 2–3 days, supporting generalizability of these dosing intervals.

In summary, clone M/K-2.7 is most commonly dosed at 0.1–0.2 mg per mouse via intraperitoneal injection every two days for up to 14 days, but researchers may adjust the regimen based on the experimental mouse model and desired effect.