BKV
Our most advanced program, SPK004, a monoclonal antibody, targets BK polyomavirus (“BKPyV”) infection in kidney transplant recipients.
Medical Need
BK polyomavirus is present in more than 80% of the general population and is typically asymptomatic, as viral replication is effectively controlled by the immune system. However, in immunosuppressed kidney transplant recipients, BKPyV can reactivate, leading to BK virus–associated nephropathy (BKVAN), which significantly increases the risk of impaired kidney function, graft loss, and reduced patient survival.
BKPyV reactivation therefore remains a major unmet medical need in kidney transplantation, as no curative treatment or vaccines are currently available. The only available clinical intervention is a reduction of immunosuppressive therapy. While this approach may partially limit viral replication, it substantially increases the risk of acute graft rejection. In addition, its antiviral efficacy is often suboptimal due to the slow recovery of immune function. As a result, patients may experience prolonged exposure to high viral loads, which is strongly associated with progressive kidney damage and an increased likelihood of graft failure or loss.
BKPyV infection in kidney transplant recipients represents a significant unmet medical need. Globally, more than 110,000 kidney transplantations are performed each year. Among these patients, approximately 20–30% experience BKPyV reactivation within the first year post-transplantation while receiving immunosuppressive therapy to prevent graft rejection.
If not adequately controlled, BKPyV reactivation can progress to BK virus-associated nephropathy (BKVAN) is one of the major causes of graft dysfunction and loss in kidney transplant recipients. Furthermore, early BKV replication after transplantation increases the risk of late acute rejection and prolonged BK virus (BKV) replication increases the risk of urothelial carcinoma in kidney transplant recipients. Sustained BKV infection is also associated to hemorrhagic cystitis in hematopoietic stem cell transplant recipients. BKV infection and associated diseases thus represent a growing medical problem as no BKV-specific antiviral therapies are available and the population of transplant recipients continues to increase
Mechanism of Action
Our lead asset, SPK004, is a proprietary monoclonal antibody targeting the BK polyomavirus (BKPyV) surface protein, resulting in the direct neutralization and elimination of viral particles.
BKPyV is a member of the Polyomaviridae family and also known as Human polyomavirus 1.
The capsid of BKPyV is composed of pentamers of a single protein, VP1, which is the only part of the virus exposed on its surface. SPK004 binds to VP1 and blocks the attachment of the virus to its target cells in the body, supporting high functionality and a high barrier to viral resistance.
SPK004
SPK004 possesses a set of differentiated attributes that support its positioning as a best-in-class therapeutic candidate. Preclinical studies demonstrate that SPK004 is a highly potent monoclonal antibody with activity against all major BKPyV genotypes (I, II, III, and IV). Importantly, SPK004 retains antiviral activity against the most frequent viral escape mutations that emerge during BKPyV reactivation.
In addition, SPK004 has been rationally engineered to enhance in vivo persistence, enabling less frequent dosing (e.g., quarterly administration) while maintaining sustained, high antibody concentrations at the site of infection, particularly in the kidney. This profile is expected to improve patient convenience, ensure continuous viral suppression, and support durable clinical efficacy.