Affivant is dedicated to developing novel immune-oncology approaches to activate and enable the innate immune system to fight cancer.

Our innovative bi-specific innate cell engagers are designed to target specific patient populations as powerful monotherapies and combination treatments.
ABOUT US
Management Team Board Members

Markus Rohrwild

Chief Executive Officer

Zoë Johnson

Chief Scientific Officer

Martin Stern

Chief Medical Officer

Maximilien Murone

Vice President, Operations

Andreas Schuh

Vice President, Finance

Eric Gaukel

Nonclinical Development

Wendy Luo

Toxicology

Dan Patterson

CMC Biologics

Laura Beni

Clinical Operations

Bhavik Manocha

CMC Operations

Angela Johnson

Regulatory Affairs

Sudhir Penugonda

Clinical Development

Meret Martin-Facklam

Clinical Pharmacology

Brenton Smith

Program Management

Nanxiang Ge

Biometrics & Data Management

Peter Sandy

Translational Medicine

Nicolò Rigamonti

Cancer Immunology

Anja Bagutti

Team Coordinator

Will Gaines

Rotational Analyst

Cedric Kessler

Controller

Markus Rohrwild

Chief Executive Officer

Frank Torti, MD

Vant Chair, Roivant Sciences

Eric Venker, MD

President & Chief Operating Officer, Roivant Sciences
OUR SCIENCE

NK cells are the primary orchestrator of immune responses to solid tumors

NK cells, in contrast to CD8+ T cells, do not require activation by a specific T-cell receptor tumor cell antigen interaction. Instead, the individual's collected population of NK cells, with an extensive diversity of expression of different activating and inhibiting receptors all coded in the germline, are "licensed" by prior interaction with a diversity of normal cells, to recognize and destroy abnormal cells using non-antigenic cues such as loss of surface HLA expression.
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NK cells are the primary orchestrator of immune responses to solid tumors

NK cells, in contrast to CD8+ T cells, do not require activation by a specific T-cell receptor tumor cell antigen interaction. Instead, the individual's collected population of NK cells, with an extensive diversity of expression of different activating and inhibiting receptors all coded in the germline, are "licensed" by prior interaction with a diversity of normal cells, to recognize and destroy abnormal cells using non-antigenic cues such as loss of surface HLA expression. NK cells occur in two general ontogenies, CD56 "dim" and CD56 "bright", which appear to have different functions. CD56 dim cells cause direct tumor cell killing mediated via cell-cell contact and granzyme; CD56 bright cells, upon activation, release chemokines and cytokines to attract the infiltration of dendritic and CD8+ T cells into the tumor microenvironment, thus enabling dendritic cells to directly sample potential neoantigens in the wake of NK-dim mediated destruction. The most successful outcome of NK activation and tumor killing is both loss of tumor mass due to NK activity, along with initiation of an anti-tumor adaptive response.
Activated T cells can drive cell death after engagement of their highly specific T cell receptor alone. For therapeutic approaches like CAR-T cells, this mean that even normal cells expressing the target antigen may be killed, and thus the therapeutic index of a CAR-T therapy is highly dependent on lack of expression of the target on normal tissue. Because NK cells integrate information from many different receptors, they are far less likely to kill normal cells expressing a target antigen, and thus the therapeutic index of NK based therapies (either CAR NK or NK plus engager) is far greater than for CAR T cells.

CD16 NK engagers

NK cells may engage targets using antibodies. To do this, the antibody binds CD16 on the NK cell and its target on the target cell. The natural CD16-antibody interaction, via the antibody Fc region, is of moderate affinity. NK cell engagers are modified antibodies which bind CD16 many-fold more strongly than antibodies, while having similar affinity for target. These engagers increase the level of NK cell surveillance and effective engagement of target tumor cells. Among possible activating receptors on NK cells, CD16 engagement is unique in being able to activate resting NK cells. As measured by so called ADCC (Antibody Dependent Cellular Cytotoxicity) assays, NK engagers can induce NK mediated killing of target cells at doses several orders of magnitude lower than for antibodies to the same target. While an antibody driven interaction is not required for NK detection and killing of tumor cells in vivo, simultaneous engagement of NK CD16 and a tumor target greatly increases the time and extent to which tumor cells are surveilled by NK cells capable of killing them.
In addition to NK cells, cells of the monocyte/macrophage lineage also express CD16. These cells are abundant in the tumor microenvironment. When tested in vitro, CD16 NK engagers can also induce some macrophages to phagocytose cancer cells (Antibody Dependent Cellular Phagocytosis, ADCP). This activity may contribute to anti-tumor efficacy in vivo.

Combination therapies

The efficacy of immune therapies can often be improved by using strategically chosen combinations. As well as assessing the efficacy of NKCEs alone, we will test them in combination with NK cell infusions, checkpoint inhibitors, and other modalities of therapy.

Our Pipeline

AFVT-2101 is a third generation CD16 engager with a target that is highly overexpressed on a variety of different epithelial tumors. This molecule is in IND enabling studies and will ultimately be tested in several indications, including Ovarian, Lung, Kidney and Breast cancers.
Roivant Sciences, Inc. (2022) Affivant to Present Data on AFVT-2101 at 37th Annual Meeting of SITC
Ahmad Trad, Michael Tomaszowski, Josef Caslavsky, Robert Freitag, Sudhir Penugonda, Keith Haan, Markus Rohrwild, Daniel O’Shannessy, Jana Siegler, Peter Sandy, Eric Gaukel, Uwe Reusch, Daniela Penston, Zoë Johnson (2022). AFVT-2101: an innate immune-cell engager that selectively targets FRα expressing tumor cells to safely harness potent anti-cancer responses
Demaria, O., Gauthier, L., Debroas, G., and Vivier, E. (2021). Natural killer cell engagers in cancer immunotherapy: Next generation of immuno‐oncology treatments. Eur J Immunol 51, 1934–1942.
Wingert, S., Reusch, U., Knackmuss, S., Kluge, M., Damrat, M., Pahl, J., Schniegler-Mattox, U., Mueller, T., Fucek, I., Ellwanger, K., et al. (2021). Preclinical evaluation of AFM24, a novel CD16A-specific innate immune cell engager targeting EGFR-positive tumors. Mabs 13, 1950264.
Zhang, S., Liu, W., Hu, B., Wang, P., Lv, X., Chen, S., and Shao, Z. (2020). Prognostic Significance of Tumor-Infiltrating Natural Killer Cells in Solid Tumors: A Systematic Review and Meta-Analysis. Front Immunol 11, 1242.
Huntington, N.D., Cursons, J., and Rautela, J. (2020). The cancer–natural killer cell immunity cycle. Nat Rev Cancer 20, 437–454.
Hu, W., Wang, G., Huang, D., Sui, M., and Xu, Y. (2019). Cancer Immunotherapy Based on Natural Killer Cells: Current Progress and New Opportunities. Front Immunol 10, 1205.
Long, E.O., Kim, H.S., Liu, D., Peterson, M.E., and Rajagopalan, S. (2013). Controlling Natural Killer Cell Responses: Integration of Signals for Activation and Inhibition. Immunology 31, 227–258.

Affivant empowers a global team of innovators in the biopharmaceutical industry to expand the world of treatable conditions.

With offices in New York City and Basel as well as remote working options, collaborating on a better future together has never been easier.
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