The HTRS Mid-Career Research Award is for clinicians, physician-scientists, or discovery-based scientists (MDs, DOs, PhDs, or MD/PhDs) with 5-to-15 years of academic research experience.
It provides $216,000 in funding for two-year clinical, translational, or basic science research projects in hemostasis and/or thrombosis and is designed to assist recipients in making the transition to full academic research independence and R01-equivalent funding. Eligible applicants must demonstrate a commitment to academic research careers in classical hematology and fulfill the following requirements: have an MD, DO, PhD, MD/PhD, or equivalent doctoral degree, hold an academic faculty position at an institution in the U.S. or Canada, have had significant career development award funding, be working toward and eligible to receive a first R01 or equivalent in the U.S. or Canada, and demonstrate a clear path by which the MCRA will support submission of an R01 or equivalent in the U.S. or Canada.
Click Here for the Request for Applications
Total Award
$216,000 USD over 2 years
Requirements
Award seekers must be HTRS Core-level members in good standing at the time of application.
Status & Deadlines
Letters of Intent Deadline: Friday, October 24, 2025 at 11:59 PM ET
Full Proposal Deadline: Friday, January 23, 2026 at 11:59 PM ET
Not a Member?
Visit the HTRS Membership Page to join.
2025 Mid-Career Research Award Recipient
Award Recipient
GLAIVY BATSULI, MD
Assistant Professor | Stanford University
2025 HTRS Mid-Career Research Award
Funded by HTRS
Project Title:
“Elucidating Mechanisms of the B Cell Response in Factor IX Inhibitor Development”
HTRS MCRA Description of Aims
Proposal Title: Elucidating Mechanisms of the B Cell Response in Factor IX Inhibitor Development
Formation of neutralizing antibodies, called inhibitors, against coagulation protein factor IX (FIX) and the associated risk of life-threatening anaphylaxis is a distinct complication of hemophilia B management not commonly observed in other inherited clotting factor deficiencies. The risk of anaphylaxis with FIX re-exposure also restricts the utility of traditional immune tolerance induction methods for inhibitor eradication.
This proposal will investigate the hypothesis that Tfh13 cell activation is required for the development of high-affinity IgG and IgE associated with anaphylaxis in FIX inhibitor development. In order to test this hypothesis, the following 2 aims will be assessed:
- Define the Tfh cell population that mediates production of FIX-specific antibodies.
- Determine the evolution of the antibody repertoire with FIX humoral immune responses.
The long-term goal of this work is to elucidate the immune pathways that mediate antibody responses favoring anaphylactic reactions in order to identify therapeutic targets for FIX tolerance induction.