Anti-Mouse CD1d Antibody (1B1)

製品番号: HY-P992059: Data Sheet
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Anti-Mouse CD1d Antibody (1B1) is an antibody targeting mouse CD1d (K_d=12.5 nM). By inserting into the lipid-binding groove of CD1d, Anti-Mouse CD1d Antibody (1B1) overlaps with the binding sites of type I and type II NKT cell receptors (TCR), thereby effectively blocking TCR-mediated interactions. Anti-Mouse CD1d Antibody (1B1) activates antigen-presenting cells such as dendritic cells and macrophages, induces them to release IL-12p70, and increases the levels of key cytokines including IL-12, IFN-γ and IFN-α in mouse serum. Anti-Mouse CD1d Antibody (1B1) can be used in studies related to renal cancer, breast cancer and colon adenocarcinoma. When combined with anti-DR5 or anti-CD137 antibodies and chemotherapeutic drugs, Anti-Mouse CD1d Antibody (1B1) exhibits significant tumor inhibitory and even eradication effects in mice.

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Anti-Mouse CD1d Antibody (1B1) 構造式

容量		在庫状況
MOQ		Minimum order quantity
1 mg		お問い合わせ
5 mg		お問い合わせ
10 mg		お問い合わせ
Other size		お問い合わせ

* アイテムを追加する前、数量をご選択ください

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製品説明

Isotype

Rat IgG2b

Recommend Isotype Controls

Rat IgG2b kappa, Isotype Control

Species Reactivity

Mouse

IC₅₀ & Target

CD1d

12.5 nM (Kd)

体外実験

Anti-Mouse CD1d Antibody (1B1) (overnight) binds to insect cell-expressed mouse CD1d presenting endogenous lipid, sulfatide, or GT1b with similar affinity, with K_d values ranging from 10.2 to 12.6 nM^[2].
Anti-Mouse CD1d Antibody (1B1) (2 h, overnight) blocks Type I NKT 1.2 and Type II NKT XV19 hybridoma activation by α-GalCer and sulfatide, respectively, but does not block activation by α-GSA[26,P5p]; 1B1 IgG blocks activation of both hybridomas by all three tested glycolipids, including α-GSA[26,P5p], at concentrations as low as 1.5 μg/mL^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

体内実験

1DMab therapy with Anti-Mouse CD1d Antibody (1B1) (intraperitoneal injection; 3 administrations; dose: 12.5-400 μg) induces dose-dependent clearance of established R331 renal cell carcinoma tumors in BALB/c mice. This effect is completely dependent on CD8⁺ T cells, IFN-γ, IL-12 and CD1d, and partially dependent on NK cells^[1].
1DMab therapy with Anti-Mouse CD1d Antibody (1B1) (i.p.; 200 μg; 3 administrations) efficiently eliminates established 4T1 breast cancer in BALB/c mice, and remains effective even when administration is delayed until the tumors reach a large volume; this therapy is completely dependent on CD8⁺ T cells and IFN-γ, independent of type I NKT cells, and only partially dependent on NK cells and IL-12^[1].
1DMab therapy with Anti-Mouse CD1d Antibody (1B1) (200 μg; intraperitoneal injection; 3 administrations) effectively eliminates established CT26L5 colon adenocarcinoma in BALB/c mice. This effect is completely dependent on CD8⁺ T cells and IFN-γ, independent of type I NKT cells or NK cells, and only partially dependent on IL-12^[1].
The 1DMab therapy with Anti-Mouse CD1d Antibody (1B1) (200 μg; i.p.; administered 3 times on days 19, 23, and 27) exhibits better efficacy than the combination therapy of Doxorubicin (HY-15142A) + anti-CD1d + anti-CD137 in eradicating established late-stage 4T1 breast cancer in BALB/c mice^[1].
1DMab therapy with Anti-Mouse CD1d Antibody (1B1) (i.p.; 200 μg; administered 3 times on days 19, 23 and 27) exhibits superior efficacy over the combination therapy of Gemcitabine (HY-17026) + anti-CD1d + anti-CD137 and other tested chemoimmunotherapies in eliminating established advanced CT26L5 colon adenocarcinoma in BALB/c mice^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	BALB/c wild-type; BALB/c Jα18^−/−; BALB/c CD1d^−/− (female, >6 weeks old, subcutaneous inoculation with R331 renal carcinoma cells)^[1]
Dosage:	12.5-400 μg (dose-dependent tumor eradication); 200 μg (delayed treatment; cell depletion; cytokine neutralization)
Administration:	i.p.; 3 doses on days 7,11,15; 3 doses on days 11,15,19; 3 doses on days 15,19,23; 3 doses on days 19,23,27
Result:	Resulted in 40% tumor eradication when 200 μg treatment delayed to day 11, 20% when delayed to day 15, and 0% cures (only tumor growth suppression) when delayed to day 19. Completely lost tumor suppressive activity (0% cures) with 200 μg in CD8⁺ T cell-depleted mice. Suppressed tumor growth but resulted in 0% cures with 200 μg in NK cell-depleted mice. Failed to suppress tumor growth (0% cures) with 200 μg in CD1d^−/− mice. Resulted in 0% cures with 200 μg in mice treated with neutralizing anti-IFN-γ or anti-IL-12 mAbs.

Animal Model:	BALB/c wild-type; BALB/c Jα18^−/− (female, >6 weeks old, subcutaneous inoculation with CT26L5 colon carcinoma cells)^[1]
Dosage:	200 μg
Administration:	i.p.; 3 doses on days 7,11,15; 3 doses on days 15,19,23; 3 doses on days 19,23,27; 3 doses on days 27,31,35
Result:	Completely lost tumor suppressive activity (0% cures) in CD8⁺ T cell-depleted mice or mice treated with neutralizing anti-IFN-γ mAbs. Suppressed tumor growth and maintained 60% (3/5) tumor eradication in NK cell-depleted mice. Suppressed tumor growth with 20% tumor eradication in mice treated with neutralizing anti-IL-12 mAbs. Induced 100% tumor eradication in Jα18^−/− mice (lacking type I NKT cells), comparable to wild-type mice.

Gene ID

12479 [NCBI]

Accession

P11609

Target

CD1d

Application

ELISA, FACS, Functional assay, Research in vivo

Conjugated

Unconjugated

Reconsititution

The product can be reconstituted/diluted with sterile PBS or saline.

SMILES

[Anti-Mouse CD1d Antibody (1B1)]

Formulation

Please refer to the lot-specific COA for specific buffer information.

保管条件

Please store the product under the recommended conditions in the Certificate of Analysis.

純度とドキュメンテーション

Inhibitory Antibodies User Guide (603 KB)

参考文献

[1]. Teng MW, et al. CD1d-based combination therapy eradicates established tumors in mice. J Immunol. 2009 Aug 1;183(3):1911-20. [Content Brief]

[2]. Ying G, et al. Structural basis of NKT cell inhibition using the T-cell receptor-blocking anti-CD1d antibody 1B1. J Biol Chem. 2019 Aug 30;294(35):12947-12956. [Content Brief]