Immuron Ltd — Regulatory Filings 2009

Nov 10, 2009

10 November 2009

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ASX Release

Immuron Limited ABN 80 063 114 045

Corporate Details:

ASX Code: IMC OTCQX Code: IMROY (U.S.)

Directors:

Significant Progress in Treatment of Metabolic Syndrome

Following our announcement on 2[nd] November in respect of the joint Hadassah/Immuron research on Oral Immunotherapy, we attach a copy of the abstract published in the proceedings of the American Liver Disease Association conference.

Chairman:

Prof. Colin Chapman Non-Executive Directors: Prof. Roy Robins-Browne Mr. Arie Nudel Mr. Simon Sallka

General Manager Research & Development

Dr Grant Rawlin

Substantial Shareholders:
Hadasit Medical Research	19.8%
Alaven Consumer H’care	3.8%
Tatura Milk Industries	2.7%

The authors presented data showing the effectiveness of Immuron’s anti-insulin antibodies in improving or reversing important markers of Metabolic syndrome in an animal model. This study focused on Fatty Liver disease (NASH).

NASH is the most common liver disease in the western world and it is estimated that between 2-5% of adults in the USA suffer from it. Currently there is no effective drug treatment for NASH.

Our research indicated that there were significant improvements in certain metabolic markers such as, glucose levels, liver damage, and insulin levels after the antibody based oral therapy was used for two weeks.

Following the significant success of these animal trials we are preparing to conduct human trials within the next three months at the Hadassah Medical Centre’s clinical trial unit in Jerusalem.

Contact Details:

Immuron Limited Level 1 39 Leveson Street North Melbourne VIC 3051 Australia

Tel: +61 (0)3 9018 4880 Fax: +61 (0)3 9018 4881

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Dr Grant Rawlin General Manager Research & Development

Website: www.immuron.com

Extract of Presentation to The American Association for the Study of Liver Diseases, The Liver Meeting, Boston, USA. The abstract is published in Hepatology 50: 300A (Suppl 4), 2009

Promotion Of CD4+CD25+FOXP3+ And Suppression Of Th17 Lymphocytes In The Adipose Tissue Alleviates The Hepatic Damage And Insulin Resistance In NASH: An Active Role Of The Adipose Tissue In Regulating The Hepatic Injury

Tomer Adar, Gadi Lalazar, Ami Ben Ya'acov, Madi El Haj, Meir Mizrahi, Yehudit Shabat, Yoav Lichtenstein, Dimitri Kanovich , Yaron Ilan[1] 1Liver Unit, Department of Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel

Introduction : Regulatory T cells (Tregs) are recognized as an important immunomodulatory component of the adaptive immune system. Immune dysregulation may lead to chronic inflammation, triggering chronic insulin insensitivity and nonalcoholic steatohepatitis (NASH). The role of Tregs in the adipose tissue in the regulation of NASH was not previously studied. Aim: To assess the effects of Tregs stimulation on hepatic injury and insulin resistance in NASH. Methods: Leptin deficient Ob/Ob mice were fed for 4 weeks with colostrum derived solutions (CDS) enriched with anti insulin specific antibodies (AIS-CDS, Immuron, Australia), or with purified anti insulin specific CDS (PAIS-CDS). The immunologic effect on the adipose tissue was determined by flow cytometry performed on the central adipose tissue and its stromal vasculature (SV), and compared with the effect on immune system of the liver and the spleen. Hepatic injury and insulin resistance was determined by glucose tolerance tests (GTT) and liver enzymes. Results: Oral administration of anti-insulin antibodies promoted the SV CD4+CD25+FoxP3+ cells (13.05 vs. 27.94 p=0.01). Treatment was associated with a decrease of the CD4+IL17+ lymphocyte subset in the adipose tissue (87.89 vs. 12.93, p<0.01), the SV (61.86 vs. 14.99, p<0.01), and in the liver (40.18 vs. 2.66, p<0.01). The liver CD8+CD25+FoxP3+ lymphocyte subset was significantly increased (0.36 vs. 2.39, p<0.05). Promotion Tregs in the adipose tissue was accompanied by a marked improvement in insulin resistance manifested by decreased glucose and insulin serum levels, and improved glucose tolerance test results (a decrease of 45%, in the area under the curve 23355 vs. 42448, in treated vs. controls, respectively), along with decreased liver enzymes (ALT levels decreased from 743.4 to 379.8 IU, p<0.05; and AST from 770.5 to 299IU, in controls vs., treated respectively, p=0.07) without a change in body weight. Conclusions: The immune system of the adipose tissue plays an important role in the regulation of the metabolic syndrome. Decreasing TH17 in the liver, adipose tissue and SV, along with promotion of CD4+CD25+FoxP3+ and CD8+CD25+FoxP3+ Tregs (in the SC and liver respectively), by oral administration of anti insulin CDS offers a new treatment modality for NASH and insulin resistance, making Tregs in adipose tissue as a new therapeutic target for alleviation of the liver damage in NASH.