AMENDMENT TO THE RESEARCH AND DEVELOPMENT AGREEMENT BETWEEN THE BRIGHAM AND WOMENS HOSPITAL, INC. AND AUTOIMMUNE, INC. (A5732)

Exhibit 10.1

AMENDMENT TO THE RESEARCH AND DEVELOPMENT AGREEMENT

BETWEEN

THE BRIGHAM AND WOMEN’S HOSPITAL, INC. AND AUTOIMMUNE, INC.

(A5732)

This Amendment to the Research and Development Agreement (“Amendment”) between The Brigham and Women’s Hospital, Inc. (“BWH”) and AutoImmune, Inc. (“Company”) is effective July 1, 2003. The BWH and the Company are parties to a Research and Development Agreement effective September 9, 1988, as amended and restated on July 1, 1992, April 14, 1995, July 1, 2000, July 1, 2001 and July 1, 2002 (“Agreement”), pursuant to which the BWH agreed to conduct certain scientific research in consideration of the payment of certain fees by the Company.

BWH and Company now wish to amend certain provisions of the Agreement, and in consideration of the promises and agreements set forth herein, and for other good and valuable consideration, the BWH and Company hereby agree as follows:

$12,000 due upon execution of this Amendment;

$12,000 due October 1, 2002;

$12,000 due January 1, 2003;

$12,000 due April 1, 2003

Except as expressly modified above, all obligations in the Agreement remain in full force and effect.

IN WITNESS WHEREOF, the parties hereto have caused this Amendment to be executed by their duly authorized representatives effective as of the first date written above.

Date: 10/8/03

Appendix A1: Immunologic approach to decrease myocardial inschemia-reperfusion injury

Background: Myocardial ischemia-reperfusion (MI/R) injury is appreciated as a potent stimulus for tissue destruction and possible cardiac failure. Infarctions link to MI/R are the most common cause of death in the western world and also in the developing world. Recent evidence shows that acute MI/R is associated with intense inflammatory reaction: as neutrophils and monocytes, that play a part in both acute extension of injury and repair of the myocardium.

Experimental Design: The inflammatory reaction produces a vast array of mediators over the course of the inflammation. Several works in the literature attempted to control inflammation both in the brain or the peripheral tissue by inducing tolerance to autoantigens as myelin basic protein (MBP). Oral and nasal tolerance, are well established models whereby immunologic tolerance is induced to a specific antigen through administration of specific antigen. Upon restimulation with the appropriate antigen, T-cells in animals tolerated with a low-dose regimen secrete cytokines such as transforming growth factor ß1 (TGF-ß1) or IL-10 that are a potent anti-inflammatory cytokines with tissue protective properties. This tolerance may lead to relatively organ specific immunosuppression. Therefore, active immunologic tolerance to heart antigens, such as troponin T, could decrease myocardial inflammation and improve outcome after MI/R through organ-specific immunosuppression. In these experiments we will have three specific goals:

Appendix B1

Contract Budget 07/01/2003 – 06/30/2004