Why Both Innate and Adaptive Immunity Matter in Cancer
Durable cancer immunotherapy depends on more than activating T cells alone. Clinical experience increasingly shows that effective and lasting antitumor responses require coordinated engagement of both the innate and adaptive immune systems, with innate immunity playing a critical role in initiating, shaping, and sustaining adaptive responses.
Plasmacytoid dendritic cells sit at the center of this coordination. When activated, pDCs produce Type I and Type III interferons that enhance antigen presentation, recruit and activate natural killer cells, and support the priming, expansion, and function of cytotoxic T cells. In this way, pDCs serve as a biological bridge—linking early immune sensing to durable, antigen-specific adaptive immunity.
Importantly, this approach is not simply interferon therapy. Rather than administering interferon directly, pDC activation allows interferon signaling to be generated locally, transiently, and in coordination with other immune signals as part of a broader, physiologic immune response. This distinction is critical to both immune effectiveness and clinical practicality.
Much of this immune orchestration occurs within lymph nodes, where tumor antigens are processed, immune memory is formed, and adaptive immune responses are programmed. Across multiple clinical settings, it has now been demonstrated that preserving lymph nodes at the time immunotherapy is delivered can meaningfully enhance immune priming and long-term benefit.
Because lymph nodes function as systemic immune hubs, maximizing their contribution to cancer immunity requires therapies capable of generating systemic immune responses, rather than approaches that act exclusively within the tumor microenvironment.
Why Sustained Systemic TLR7 Activation Is Important
Systemic activation of TLR7 has historically been challenging in the clinic. Earlier approaches often triggered broad inflammatory signaling, including activation of NF-κB–driven pathways, which limited tolerability and constrained clinical utility.
In some cases, this generalized activation also extended to counter-regulatory and immunosuppressive immune cell populations, which limited effective antitumor immune responses.
PRTX007 was designed with a different objective: to favor interferon-associated innate immune programs that support antitumor activity, while minimizing engagement of inflammatory pathways that undermine clinical tolerability and activity. This more selective pattern of immune activation reflects deliberate choices in molecular design and dosing strategy, aimed at achieving effective systemic immune engagement without unnecessary immune activation.
PRTX007: Designed for Systemic Cancer Immunotherapy
In early clinical studies in healthy volunteers, PRTX007 demonstrated consistent systemic immune engagement aligned with activation of innate immune pathways and was generally well tolerated. Preclinical studies further support systemic distribution and immune activation without widespread pro-inflammatory cytokine release.
These characteristics position PRTX007 as a promising immunotherapy candidate for oncology applications where systemic immune activation and intact lymph node function are central to therapeutic benefit—including combination strategies with immune checkpoint inhibitors, neoadjuvant and adjuvant treatment settings, and approaches focused on eliminating minimal residual disease.
Primmune’s strategy is to develop PRTX007 as a broadly applicable immune-activating therapy that complements existing standards of care and helps unlock the full potential of cancer immunotherapy.
PRTX007: Clinical Validation of Primmune’s TLR7 Agonist
PRTX007 is a novel, orally administered, systemically active toll-like receptor 7 (TLR7) agonist designed in-house at Primmune to functionally tune immune signaling toward interferon-associated innate immune programs, while minimizing engagement of pro-inflammatory pathways that have historically limited the clinical utility of systemically acting TLR7, TLR7/8, and TLR8 agonists.
PRTX007 has been administered to 119 healthy volunteers across two Phase 1 clinical studies (Study PRTX007-001 and Study PRTX007-002). In these studies, PRTX007 demonstrated consistent systemic immune engagement aligned with interferon-driven signaling, without the broad pro-inflammatory responses that limited earlier approaches. PRTX007 was generally well tolerated, and no serious adverse events were observed.
Preclinical studies further support the systemic distribution and activation of target immune cells and the ability to sustain immune engagement without inducing widespread pro-inflammatory cytokine signaling.
Together, published clinical data from Study 001 and additional data from Study 002 demonstrate:
- A favorable safety profile, with no apparent overlapping mechanistic toxicity relative to known immune checkpoint inhibitors
- Dose-dependent systemic exposure and activation of innate immune pathways without induction of broad pro-inflammatory cytokines
- Breadth of immune induction with coordinated downstream engagement of adaptive immune responses
Click here for publications highlighting Primmune’s published clinical data.
Team
Our team is committed to the invention of new medicines to treat people suffering from cancer and to creating substantial value for our investors and partners. Whenever possible, we aim to cure cancers and eradicate minimal residual disease in multiple different tumor types. Primmune brings together deep experience across the science and business of drug discovery, development, and commercialization to improve outcomes for patients.
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Primmune Therapeutics, Inc.
2011 Palomar Airport Rd, Suite 101
Carlsbad CA 92011