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You won’t see EpiVax in Prague this February. And you won’t hear about EpiVax’ new tolerizing technology in Boston unless you come a day early to the Tregitope meeting. And we won’t be at IBC in Tokyo, nor at IIR in San Francisco. Why?

Because, we’re scientists with great new information on tolerance induction and immunogenicity reduction to share, and on principle, EpiVax will not pay to speak. We don’t believe that you go to conferences to hear info-mercials . . . we believe that you want an open and honest exchange of ideas because you want to move the science of immunogenicity forward.

Why not pay to speak, like so many of our competitors do? The conflict is inherent in the speaking fee. In clinical medicine, all monies paid by Pharma companies to support publication of scientific contents have to be declared. Speakers, and writers, cannot proclaim without disclaimers (declaring their financial support). Why should discovery science different from clinical science? Don’t you deserve to know who, on the agenda in Prague and in Boston, is paying upwards of $5,000 for the privilege of to speaking to you?

How do commercial conferences work? Take big names and salt them liberally on the advisory board. Butter the Internet with invitations to speak. Toss in a few academics. Cook up an agenda, saving choice slots for paying players.  Make the abstract selection process opaque. Ignore advances in the field. The result? A commercial, but not a scientific success.

This is a call for full disclosure when it comes to commercial conferences. Clinical conferences practice this. Why should drug discovery conferences be any different? We don’t think they should be.

OK, we’ve made our full disclosure. We don’t pay to speak. Now . . . It’s up to you. You’ve paid to attend. You deserve it. Ask the commercial conference company for the full Monty. Ask them to put the prices on the agenda. Find out which speaker is lobbying you, rather than sharing good science.

In the meantime, if you want to hear about Tregitope then join us (for free) in Boston on May 16th, at the Westin Copley. Email Shannon Pelletier spelletier@epivax.com and we’ll reserve your seat.

Here’s the abstract from a talk that we’d gladly give – you name the venue – but only if we can give it for free:

Immunogenicity and tolerance: putting recent immunology research to work when developing better protein therapeutics

A. S. De Groot1,2,3, J. Buhlmann1, D. W. Scott4, Bill Martin1

1EpiVax, Inc., 2University of Rhode Island,

3Brown University Medical School, 4University of Maryland

The contributions of effector T cell epitopes to clinical immunogenicity and autoimmunity are now broadly accepted. Pre-clinical efforts are therefore directed towards modulating the presence of T cell epitopes in protein therapeutics by screening for epitopes and deimmunizing (removing T cell epitopes) prior to further development of the protein for clinical use. In allergy and autoimmunity, efforts are directed at broad suppression of cell-mediated immune responses. The discovery of natural regulatory T cell epitopes in the sequence of therapeutic mAbs represents a paradigm shift for protein therapeutics, allergy, autoimmunity and transplantation. These natural Treg epitopes (also known as Tregitopes) are promiscuous MHC Class II T cell epitopes located in the Fc and framework regions of Fab from IgG.

Methods. The Tregitopes have been evaluated in vitro and in vivo in five collaborating laboratories. Investigations in allergy (OVA model), transplantation (MLR, cardiac transplant model), protein therapeutics (OVA, FVIII) and autoimmunity (EAE, NOD) have demonstrated that tolerance to a range of antigens can be induced by co-administration of the Tregitopes with the target antigens.

Results. Tetramer staining confirms thatTregitopes specifically activate CD4+CD25+FoxP3+ natural regulatory T cells (nTregs). In vitro, co-incubation of antigens with “Tregitopes” in vitro leads to suppression of effector cytokine and chemokine secretion, reduced proliferation of effector T cells, and expansion of antigen-specific adaptive Tregs (aTregs). In vivo, co-administration of Tregitopes with a range of proteins (such as FVIII, thyroid stimulating hormone receptor, ovalbumin, and autoantigens) leads to suppression of T cell and antibody responses to the test antigens. Differences in the Tregitope content of monoclonal therapeutics such as ofatumumab and rituximab, humira and infliximab, explain differences observed in the clinical setting.

Conclusion. This talk will describe recent laboratory studies and conclude with a discussion of the role of Tregitopes in the design of safer, more effective protein therapeutics, whether these proteins are monoclonal antibodies, novel scaffolds, replacement therapies or biosimilars. The therapeutic implications for the fields of allergy, autoimmunity and transplantation will also be described. Four case studies will be presented (FPX, Ofatumumab, Humira, and FVIII). Regulatory T cell induction in the context of protein therapy and inflammation may contribute to the design of improved biologic therapeutics for a wide range of clinical conditions.