| Name | Leukadherin-1 |
| Description | Leukadherin-1 is an allosteric activator of CD11b/CD18. Increasing CD11b/CD18-dependent cell adhesion to fibrinogen, Decreasing leukocyte motility and transendothelial migration; reduces inflammation. |
| Cell Research | NK cell stimuli (where used) were added as follows: (1) Syk inhibitor (1 μM), (2) Leukadherin-1 or dimethylsulphoxide (DMSO) (vector control) (7.5 μM). Shown to induce ∼82% of maximum response with negligible off-target effect, (3) anti-CD210 or isotype control (5 µg/ml), (4) 30-45 min after Leukadherin‐1 NK cells were stimulated with combinations of IL-12 (10 ng/ml), IL-15 (30 ng/ml) or IL-18 (10 ng/ml): either IL-12 + IL-15 or IL-12 + IL-18. Monocytes were stimulated using pam3csk4 (TLR-2 agonist, 300 ng/ml) or R848 (TLR-7/8 agonist, 2 µg/ml). Supernatants were stored at −80ºC for < 1 month before quantification. To exclude non-specific Leukadherin-1-mediated cytotoxicity, cell viability is assessed at 24 h using the CellTitre-Glo reagent. (Only for Reference) |
| In vitro | Leukadherin-1 pretreatment reduces secretion of interferon (IFN)-γ, tumour necrosis factor (TNF) and macrophage inflammatory protein (MIP)-1β by monokine-stimulated NK cells. It also reduces secretion of IL-1β, IL-6 and TNF by Toll-like receptor (TLR)-2 and TLR-7/8-stimulated monocytes. Leukadherin-1 modulates NK cell cytokine secretion and does not modulate Syk activation in NK cells[1]. LA1 increases CD11b/CD18-dependent cell adhesion to fibrinogen with 50% effective concentration (EC50, the effective concentration for a 50% increase in adhesion) values of 4 μM[3]. |
| In vivo | Leukadherin-1 has potent anti-inflammatory effects in a range of animal models, including an autoimmune nephritis model, without obvious short-term side effects[1]. Leukadherin-1 (LA1) increases leukocyte adhesion, preventing their transmigration and tissue recruitment in vivo. LA1 treatment reduces interstitial leukocyte infiltration in the allograft, reduces neointimal hyperplasia and glomerular damage, and prolongs graft survival from 48.5% (CsA only) to 100% (CsA and LA1) on day 60 in a mouse model of fully MHC-mismatched orthotopic kidney transplantation[2]. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | H2O : < 1 mg/mL (insoluble or slightly soluble)
Ethanol : < 1 mg/mL (insoluble or slightly soluble)
DMSO : 15 mg/mL (35.59 mM), Sonication is recommended.
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| Keywords | αMβ2 | vascular | Mac-1 | leukocyte | Leukadherin-1 | Leukadherin1 | Leukadherin 1 | Integrin | Inhibitor | inhibit | inflammatory | ICAM-1 | endothelium | CR3 | ComplementSystem | Complement System | CD11b/CD18 | adhesion |
| Inhibitors Related | Iptacopan hydrochloride | Tirofiban hydrochloride monohydrate | Iptacopan | ADH-503 | Dexamethasone acetate | Dexamethasone | CLT-28643 | Bestatin hydrochloride | Cyclosporin A | Dextran sulfate sodium salt (MW 5000) | 3-Phenoxybenzaldehyde | 2-hydroxy Flutamide |
| Related Compound Libraries | Membrane Protein-targeted Compound Library | ReFRAME Related Library | Multi-Target Compound Library | Anti-Aging Compound Library | Immunology/Inflammation Compound Library | Covalent Inhibitor Library | Cytoskeletal Signaling Pathway Compound Library | Human Metabolite Library |
United States
