Our program
IMG-007: Our differentiated anti-OX40 monoclonal antibody
IMG-007 is a next-generation anti-OX40 monoclonal antibody that has been engineered to optimize efficacy, safety, and convenience for patients. It binds with high affinity to the OX40 receptor on activated T cells, blocking OX40L binding and downstream signaling without depleting T cells. It also features an extended half-life, which may allow patient-friendly dosing.
IMG-007 has a trifecta of differentiating features
1
Receptor targeting for optimal efficacy profile
Targeting OX40 receptor (OX40) rather than OX40 ligand (OX40L) allows IMG-007 to inhibit OX40/OX40L signaling in both blood and tissues.
2
T cell-preserving for safety and tolerability
IMG-007 incorporates an engineered Fc region that silences ADCC function, meaning activated T cell signaling is attenuated, but T cells are not killed and depleted. This advantage can potentially improve tolerability and increase the therapeutic window, allowing higher dosing, more efficacy, all while maintaining safety.
3
Extended half-life for patient- and physician-friendly dosing schedules
IMG-007's engineering has resulted in a half-life of approximately 5 weeks in a patient’s bloodstream, opening the potential for dosing intervals of once every few months or beyond.
What is OX40 and what is its connection to inflammation and autoimmune disease?
OX40 is a protein found primarily on the surface of T cells, a key type of immune cells, which are essential for orchestrating the body’s defense against infections and disease. When OX40 is activated, it interacts with OX40 ligand (OX40L) which amplifies immune activity by promoting T cell survival, proliferation, and crosstalk with other immune cells. OX40 signaling can become overactive in autoimmune and inflammatory diseases. When this happens, it contributes to persistent immune activation that damages the body’s own tissues and drives chronic inflammation.
OX40 is expressed on multiple activated T cell subtypes, including Th1, Th2, Th17, and Th22 effector cells as well as long-lived memory T cells. These cells have distinct functions. OX40 activation of effector T cell populations increases the release of numerous inflammatory cytokines and chemokines, molecules that signal and sustain immune activity, which in turn amplifies inflammation. OX40 signal activation also helps maintain memory T cells that “remember” and perpetuate these harmful responses over time. This prolonged immune signaling can make diseases more severe and chronic. OX40 is also expressed on T cells that regulate immune responses, called Tregs. OX40 signaling can suppress Treg function, leading to further exacerbation of inflammation.
Because of its important role in amplifying and sustaining immune responses, OX40 has emerged as a promising therapeutic target in wide range of autoimmune and inflammatory diseases. Drugs that block OX40 binding to OX40L can potentially calm and rebalance this overactive immune circuitry without broadly suppressing the entire immune system.
Atopic dermatitis (AD, the most common type of eczema) is mainly driven by dysfunction of T cells. In AD, the OX40 axis is highly active in inflamed skin. OX40-OX40L signaling amplifies T cell responses by disrupting the balance between effector T cells and immunomodulatory Treg cells. OX40 signaling inhibition is a different approach from biologic therapies that work primarily to inhibit signaling through a single pathway. For example, anti-IL-13 or anti-IL4Rα antibodies work predominantly to block Th2 signaling. Eczema is a complex and heterogeneous disease, with different pathways involved to varying degrees in different patients. Targeting multiple T cell subtypes by blocking OX40 may have the potential to rebalance multiple dysfunctional T cell signaling pathways to address disease heterogeneity.
Our first focus: atopic dermatitis
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease marked by itching, redness, rashes, and dry or cracked skin. It often begins in childhood but can persist into adulthood, disrupting sleep, daily function, and mental health. The disease, the most common type of eczema, results from a mix of genetic predisposition, environmental triggers, skin-barrier dysfunction, and immune imbalance, including overactivation of Th1, Th2, Th17 and Th22 cell driven inflammatory pathways.
AD affects people of all ages, races and geographies; hundreds of millions of people worldwide have atopic dermatitis, including approximately 4% of all children, making it one of the most common chronic immune-mediated disorders. Cases have been steadily rising year over year. According to the National Eczema Association, it is estimated that 16.5 million adults in the U.S. have AD, with 6.6 million meeting criteria for moderate-to-severe disease. Standard care begins with topical therapies, progressing to systemic treatments such as monoclonal antibodies (biologics) or oral drugs for moderate-to-severe disease. Although several molecularly targeted therapies have been introduced into the market, real-world use remains limited, with fewer than 15% of eligible patients currently receiving such treatment. Moreover, adherence is a challenge: recent analyses show over one in three (35%) patients taking biologics for AD discontinue treatment over time, most often due to insufficient efficacy or tolerability concerns. This highlights the strong need for novel therapeutic approaches that can lead to additional treatment options for patients.
What is OX40 and what is its connection to inflammation and autoimmune disease?
OX40 is a protein found on the surface of T cells, a key type of immune cells, which are essential for orchestrating the body’s defense against infections and disease. When OX40 is activated, it amplifies immune activity by promoting T cell survival, proliferation, and crosstalk with other immune cells. While this process is critical for fighting infections or cancer, OX40 signaling can become overactive in autoimmune and inflammatory diseases. When this happens, it contributes to persistent immune activation that damages the body’s own tissues and drives chronic inflammation.
OX40 is expressed on several T cell subtypes, including Th1, Th2, and Th17 effector cells as well as long-lived memory T cells. These cells have distinct functions. OX40 activation across these populations increases the release of inflammatory cytokines, molecules that signal and sustain immune activity that amplifies inflammation. OX40 activation also helps maintain memory T cells that “remember” and perpetuate these harmful responses over time. This prolonged immune signaling can make diseases more severe and chronic.
Because of its central role in sustaining and amplifying immune responses, OX40 has emerged as an important therapeutic target in autoimmune and inflammatory diseases. Drugs that block or modulate OX40 can potentially calm this overactive immune circuitry without broadly suppressing the entire immune system. Inhibiting OX40-OX40L signaling is considered a promising novel therapeutic strategy for a wide range of inflammatory and autoimmune diseases.
In atopic dermatitis (eczema), the OX40 axis is highly active in inflamed skin, driving Th2-type inflammation and itch through cytokines like IL-4, IL-13, and IL-31. Because eczema is a complex and heterogeneous disease, with different immune compartments active in different people, it can be difficult to treat. Since OX40 acts upstream in the immune response on activated T cells, blocking its signaling may help address this heterogeneity by targeting a common driver of inflammation. This has the potential to reduce inflammation, improve skin barrier function, and prevent recurrence driven by long-lived memory T cells.
Our first focus: atopic dermatitis
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease marked by itching, redness, and dry or cracked skin. It often begins in childhood but can persist into adulthood, disrupting sleep, daily function, and mental health. The disease results from a mix of genetic predisposition, environmental triggers, skin-barrier dysfunction, and immune imbalance, most notably, but likely not exclusively, overactivation of Th2 cell driven inflammatory pathways.
AD affects of all ages, races and geographies; over 120 million people worldwide have atopic dermatitis, including 4% of all children, making it one of the most common chronic immune-mediated disorders. Cases have been steadily rising year over year. According to the National Eczema Association, it is estimated that 16.5 million adults in the U.S. have AD, with 6.6 million meeting criteria for moderate to severe disease. Standard care begins with topical therapies, progressing to systemic treatments such as monoclonal antibodies (biologics) or oral drugs for moderate-to-severe disease. Although several molecularly targeted therapies have been introduced into the market, real-world use remains limited, with companies reporting less than 15% of eligible patients currently receiving the treatment. Moreover, persistence is a challenge: recent analyses show over one in three (35%) patients taking biologics for AD discontinue treatment over time, most often due to insufficient efficacy or tolerability concerns. This highlights the strong need for novel therapeutic approaches that can lead to additional treatment options for patients.
Early clinical results
In a Phase 1b/2a clinical proof-of-concept trial in patients with moderate-to-severe atopic dermatitis, three doses of IMG-007 given over 1 month resulted in a substantial reduction of symptoms for the majority of patients. Using the EASI score, a clinical trial measure of severity of disease, as the clinical endpoint, a majority (54%) of patients reached EASI-75, meaning their disease improved by 75% or more from baseline by week 16. Almost one-third (31%) improved 90% or more (EASI-90).
IMG-007 has also been evaluated in a Phase 1b/2a clinical proof-of-concept trial in patients with alopecia areata (AA) where promising clinical activity of hair regrowth has been observed. AA is an autoimmune disease that attacks the hair follicle causing hair loss, often in irregular patterns across the scalp, face, and body, and is known for its heterogenous and chronic nature.
Across early clinical studies, IMG-007 has thus far shown a favorable emerging safety and tolerability profile. In particular, no serious adverse events were observed and there were no reports of fever (pyrexia) or chills among people treated with IMG-007.
Our ongoing clinical trial
The ADAPTIVE trial: We are currently enrolling a Phase 2b study evaluating the efficacy and safety of IMG-007 in adults with moderate-to-severe atopic dermatitis. The trial includes patients with AD new to systemic therapy as well as those who have received biologics and other systemic therapies in the past.