Anti-Rat β-2-Microglobulin Monoclonal antibody (CABT-L4291) Functional Grade

Mouse Anti-Rat β-2-Microglobulin Monoclonal antibody for IA

Specifications


Host Species
Mouse
Antibody Isotype
IgG1
Clone
4C9
Species Reactivity
Rat
Immunogen
Soluble neonatal Fc receptor (FcRn)
Conjugate
Functional Grade

Target


Alternative Names
B2M; beta-2-microglobulin; Beta-2-microglobulin; beta chain of MHC class I molecules; beta-2-microglobin; β2-MG

Citations


Have you cited CABT-L4291 in a publication? Let us know and earn a reward for your research.

Customer Reviews


Write a review, share your experiences with others and get rewarded !
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket
Product Name Cat. No. Applications Host Species Datasheet Price Add to Basket

References


Molecular insights into cell toxicity of a novel familial amyloidogenic variant of beta 2-microglobulin

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Authors: Leri, Manuela; Bemporad, Francesco; Oropesa-Nunez, Reinier; Canale, Claudio; Calamai, Martino; Nosi, Daniele; Ramazzotti, Matteo; Giorgetti, Sofia; Pavone, Francesco S.; Bellotti, Vittorio; Stefani, Massimo; Bucciantini, Monica

The first genetic variant of beta 2-microglobulin (b2M) associated with a familial form of systemic amyloidosis has been recently described. The mutated protein, carrying a substitution of Asp at position 76 with an Asn (D76N b2M), exhibits a strongly enhanced amyloidogenic tendency to aggregate with respect to the wild-type protein. In this study, we characterized the D76N b2M aggregation path and performed an unprecedented analysis of the biochemical mechanisms underlying aggregate cytotoxicity. We showed that, contrarily to what expected from other amyloid studies, early aggregates of the mutant are not the most toxic species, despite their higher surface hydrophobicity. By modulating ganglioside GM1 content in cell membrane or synthetic lipid bilayers, we confirmed the pivotal role of this lipid as aggregate recruiter favouring their cytotoxicity. We finally observed that the aggregates bind to the cell membrane inducing an alteration of its elasticity (with possible functional unbalance and cytotoxicity) in GM1-enriched domains only, thus establishing a link between aggregate-membrane contact and cell damage.

Renal Effects of Antisense-Mediated Inhibition of SGLT2

JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS

Authors: van Meer, Leonie; Moerland, Matthijs; van Dongen, Marloes; Goulouze, Bas; de Kam, Marieke; Klaassen, Erica; Cohen, Adam; Burggraaf, Jacobus

ISIS 388626 is an antisense sodium-glucose cotransporter 2 (SGLT2) inhibitor designed to treat type 2 diabetes mellitus by induction of glucosuria. ISIS 388626 was demonstrated to be safe and effective in preclinical trails in several species. We undertook the present study to evaluate the safety and efficacy of 13 weekly doses of 50, 100, and 200 mg of ISIS 388626 in humans. ISIS 388626 increased 24-hour urinary glucose excretion dose dependently with 508.9 +/- 781.45 mg/day in the 100-mg and 1299.8 +/- 1833.4 mg/day in the 200-mg cohort, versus 88.7 +/- 259.29 mg/day in the placebo group. ISIS 388626 induced a reversible increase in serum creatinine, with the largest effect after eight doses of ISIS 388626 (200 mg; 0.38 +/- 0.089 mg/dl; 44% increase over baseline). Three subjects were discontinued as a result of creatinine increases. The renal clearance test revealed no indications for impairment of glomerular filtration or renal perfusion. The creatinine increases were accompanied by a rise in the levels of urinary renal damage markers [beta-2-microglobulin (B2M), total protein, kidney injury molecule (KIM1), alpha-glutathione S-transferase (aGST), N-acetyl-beta-(D)-glucosaminidase (NAG)]. Other treatment-related adverse events included mild injection site reactions occurring in 8-19% of the subjects. In conclusion, ISIS 388626 treatment induced glucosuria at a dose level of 200 mg/week. This intended pharmacological effect was small, amounting to approximately 1% of the total amount of filtered glucose. Changes in serum and urinary markers were indicative of transient renal dysfunction, most probably of tubular origin. Whether the glucosuria is caused by specific SGLT2 inhibition or general tubular dysfunction or a combination remains uncertain.

Online Inquiry

Name:
Phone: *
E-mail Address: *
Technology Interest:
Type of Organization:
Service & Products Interested: *
Project Description:

Related Products

Related Resources

Ordering Information

Payment methods we support:
Invoice / Purchase Order
Credit card

Inquiry Basket