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Apoptosis Inhibitor of Macrophage Human ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, Biotin-labelled antibody
  • Other names:CD5 molecul-like protein
  • Species:Human
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Cat. No. Size Price

RD191328200R 96 wells (1 kit)
PubMed Product Details
Technical Data


Sandwich ELISA, Biotin-labelled antibody


Serum, Plasma-Heparin

Sample Requirements

10 ul/wel


Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Range

0.16–10.0 ng/mL

Limit of Detection

0.009 ng/mL

Intra-assay (Within-Run)

n = 8; CV = 3.6%

Inter-assay (Run-to-Run)

n = 5; CV = 6.1%

Spiking Recovery


Dilutation Linearity




  • For research use only!
  • The total assay time is less than 4 hours
  • The kit measures total AIM in serum and plasma (heparin)
  • Assay format is 96 wells
  • Standard is recombinant protein
  • Components of the kit are provided ready to use, concentrated or lyophilized

Research topic

Cardiovascular disease, Immune Response, Infection and Inflammation, Metabolic syndrome, Renal disease


Urinary trypsin inhibitor (UTI) (also called bikunin or ulinastatin) is a multivalent serine protease inhibitor synthesized and released in human urine and blood. UTI is an acidic glycoprotein, composed of 143-amino acid residues. Bikunin contains two proteinase inhibitor domains of the Kunitz type, a short connecting peptide as well as N- and C-terminal extensions 10 – 25 amino acids long. The N-terminal extension carries a chondroitin sulphate chain. Each of the Kunitz domains has a binding site for a proteinase and the amino acid residues essential for binding (Met 36 of the N-terminal domain and Arg 92 of the C-terminal domain). The total molecular weight of UTI is 25 – 26 kDa. UTI is produced by endoplasmic reticulum of hepatocytes as a precursor in which UTI is linked to α1-microglobulin. Most of the UTI in blood (90 – 98 %) occurs as a covalently linked subunit of the proteins pre-α-inhibitor and inter-α-inhibitor, respectively. In human plasma the major UTI-containing protein is inter-α-inhibitor. The total concentration of UTI in human plasma is 4 – 7 μM, of which 2 – 10 % is in free form. UTI is a positive acute phase protein. The concentration of free, uncomplexed UTI in plasma of patients with inflammatory conditions has been reported to be higher than normal. The plasma UTI level and its gene expression change under severe inflammatory conditions. In patients suffering from various nephropathies, a clear correlation between the UTI and creatinine concentrations in plasma was found, implying that the kidneys are a major site of uptake of the protein. UTI is rapidly released into urine when infection occurs and is an excellent inflammatory marker, constituting most of the urinary anti-trypsin activity. In urine, in which the level of complexed UTI is negligible, the average UTI concentration is 0.03 – 0.05 μM. The level of UTI in urine may be elevated under various pathological conditions, including pneumonia, lung emphysema, rheumatoid arthritis, cancer, and surgical trauma. It appears that UTI passes through the kidneys by glomerular filtration. Some tumour cells secrete UTI, which could contribute to the high urinary levels seen in some cancer patients.

The function of UTI has been preserved during evolution. Trypsin and other serine proteases such as trombin, chymotrypsin, kallikrein, plasmin, neutrophil elastase, cathepsin and factors IXa, Xa, XIa and XlIa are inhibited by UTI, indicating that UTI is part of the inflammatory process. Furthermore, UTI can suppress urokinase-type plasminogen activator (uPA) expression through the inhibition of protein kinase C. UTI appears to prevent organ injury by inhibiting the activity of inflammatory serine proteases. In vitro studies have demonstrated that serine protease inhibitors may have anti-inflammatory properties. UTI suppresses the infiltration of neutrophils and the release of elastase and chemical mediators from them.

Clinically, UTI is widely used as a drug for patients with acute inflammatory disorders such as pancreatitis, shock and disseminated intravascular coagulation.

References to Summary

References to Apoptosis Inhibitor of Macrophage

  • Arai S, Miyazaki T. Impacts of the apoptosis inhibitor of macrophage (AIM) on obesity-associated inflammatory diseases. Semin Immunopathol. 2014 Jan;36 (1):3-12
  • Arai S, Shelton JM, Chen M, Bradley MN, Castrillo A, Bookout AL, Mak PA, Edwards PA, Mangelsdorf DJ, Tontonoz P, Miyazaki T. A role for the apoptosis inhibitory factor AIM/Spalpha/Api6 in atherosclerosis development. Cell Metab. 2005 Mar;1 (3):201-13
  • Boes M. Role of natural and immune IgM antibodies in immune responses. Mol Immunol. 2000 Dec;37 (18):1141-9
  • Calvo J, Places L, Padilla O, Vila JM, Vives J, Bowen MA, Lozano F. Interaction of recombinant and natural soluble CD5 forms with an alternative cell surface ligand. Eur J Immunol. 1999 Jul;29 (7):2119-29
  • Gebe JA, Kiener PA, Ring HZ, Li X, Francke U, Aruffo A. Molecular cloning, mapping to human chromosome 1 q21-q23, and cell binding characteristics of Spalpha, a new member of the scavenger receptor cysteine-rich (SRCR) family of proteins. J Biol Chem. 1997 Mar 7;272 (10):6151-8
  • Hardy RR, Hayakawa K. CD5 B cells, a fetal B cell lineage. Adv Immunol. 1994;55:297-339
  • Haruta I, Kato Y, Hashimoto E, Minjares C, Kennedy S, Uto H, Yamauchi K, Kobayashi M, Yusa S, Muller U, Hayashi N, Miyazaki T. Association of AIM, a novel apoptosis inhibitory factor, with hepatitis via supporting macrophage survival and enhancing phagocytotic function of macrophages. J Biol Chem. 2001 Jun 22;276 (25):22910-4
  • Kuwata K, Watanabe H, Jiang SY, Yamamoto T, Tomiyama-Miyaji C, Abo T, Miyazaki T, Naito M. AIM inhibits apoptosis of T cells and NKT cells in Corynebacterium-induced granuloma formation in mice. Am J Pathol. 2003 Mar;162 (3):837-47
  • Mimura I, Nangaku M. The suffocating kidney: tubulointerstitial hypoxia in end-stage renal disease. Nat Rev Nephrol. 2010 Nov;6 (11):667-78
  • Miyazaki T, Kurokawa J, Arai S. AIMing at metabolic syndrome. -Towards the development of novel therapies for metabolic diseases via apoptosis inhibitor of macrophage (AIM).-. Circ J. 2011;75 (11):2522-31
  • Nakaya H, Sasamura H, Hayashi M, Saruta T. Temporary treatment of prepubescent rats with angiotensin inhibitors suppresses the development of hypertensive nephrosclerosis. J Am Soc Nephrol. 2001 Apr;12 (4):659-66
  • Sarrias MR, Padilla O, Monreal Y, Carrascal M, Abian J, Vives J, Yelamos J, Lozano F. Biochemical characterization of recombinant and circulating human Spalpha. Tissue Antigens. 2004 Apr;63 (4):335-44
  • Tissot JD, Sanchez JC, Vuadens F, Scherl A, Schifferli JA, Hochstrasser DF, Schneider P, Duchosal MA. IgM are associated to Sp alpha (CD5 antigen-like). Electrophoresis. 2002 Apr;23 (7-8):1203-6
  • Uramatsu T, Nishino T, Obata Y, Sato Y, Furusu A, Koji T, Miyazaki T, Kohno S. Involvement of apoptosis inhibitor of macrophages in a rat hypertension model with nephrosclerosis: possible mechanisms of action of olmesartan and azelnidipine. Biol Pharm Bull. 2013;36 (8):1271-7
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