Targeting unmet medical needs beyond
immune checkpoint inhibitors

- Novel macrophage activator targeting primarily on solid tumors

- Targeting Claudin 18.2 low expressors

- Reversing prior anti-PD-1 resistance

- Overcoming liver toxicities of 4-1BB targeting therapies

Our Approach

Our Approach

NextGen Novel Immuno-oncology and Targeted Drugs – Allowing Broad Proprietary Combinations

Tumor Microenvironment

Tumor Cell

  • ATN-031

    (CD24 Monoclonal Antibody)

    First-in-class molecule to enter clinical development in the oncology space
  • ATN-022

    (Claudin 18.2 ADC)

    High affinity antibody (pM)
    Strong in-vivo efficacy in extremely low Claudin 18.2 expression PDX models and patients
  • ATN-037

    (CD73 Small Molecule Inhibitor)

    Potentially best-in-class molecule
    Overcomes "hook effect" and completely inhibits CD73 and reverses anti-PD-1 resistance in patients
  • ATN-101

    (PD-L1/4-1BB Bispecific Antibody)

    Potentially best-in-class molecule
    Significant anti-tumor activity in "cold" tumors or tumors resistant to anti-PD-1/L1 treatment without liver toxicity

Pipeline Assets

Portfolio of Transformational Assets

Assets
Target
(Modality)
IND
Phase I
Phase II
First-in-class Potential
CD24
(mAb)
PERFORM
Best-in-class Potential
Claudin 18.2
(ADC)
CLINCH
CD73
(Small Molecule)
STAMINA
PD-L1/4-1BB
(Bispecific Antibody)
PROBE
Assets
Target
(Modality)
IND
Phase I
Phase II
First-in-class Potential

ATN-031

CD24
(mAb)

PERFORM
Best-in-class Potential

ATN-022

Claudin 18.2
(ADC)

CLINCH

ATN-037

CD73
(Small Molecule)

STAMINA

ATN-101

PD-L1/4-1BB
(Bispecific Antibody)

PROBE
Ongoing Trials

A Highly Synergistic and Differentiated Pipeline Comprised of Clinical Stage Assets with First and/or Best-in-Class Potential

ATN-031
ATN-022
ATN-037
ATN-101
Target and Modality
CD24 Monoclonal Antibody
Claudin 18.2 ADC
CD73 Small Molecule
PD-L1/4-1BB Bispecific Antibody
Rationale
CD24 is a cell surface protein implicated in tumor cell proliferation and immune evasion. By targeting CD24 with a monoclonal antibody, this asset aims to disrupt the immunosuppressive signaling and enhance immune-mediated tumor cell killing through macrophage-dependent tumor cell phagocytosis
Claudin 18.2 is a tumor-specific antigen overexpressed in various solid tumors, making it an ideal target for an antibody-drug conjugate. By selectively delivering a cytotoxic payload to tumor cells expressing Claudin 18.2, this asset aims to minimize systemic toxicity while maximizing anti-tumor efficacy
CD73 is an ecto-enzyme that promotes the production of immunosuppressive adenosine in the tumor microenvironment. Inhibiting CD73 with a small molecule has the potential to reverse an immunosuppressed tumor microenvironment by reducing adenosine-mediated immunosuppression and restore anti-tumor immune responses
Harnesses the power of immuno-oncology by simultaneously blocking PD-L1, a key immune checkpoint, and conditionally activating the 4-1BB costimulatory receptor on T cells. This dual approach can potentially enhance anti-tumor immune response more effectively than targeting either pathway alone while minimizing risk for 4-1BB related liver toxicity
Differentiation

First in class target

No clinical competitor

Showed mono-therapy in vivo efficacy and synergy with chemotherapy, rituximab and CPI

High affinity antibody (pM); Strong in vivo efficacy pre-clinically in Claudin 18.2 low expression PDX models

Demonstrated an excellent safety profile in GLP toxicology studies

Orally bioavailable small molecule that completely overcomes 'hook effect' common in other anti-CD73 antibodies

Tissue penetrance not achievable with mAbs

Promising preclinical efficacy as a monotherapy and strong combination potential

PD-L1 cross-linking dependent activation of 4-1BB to avoid unwanted 4-1BB signaling in normal tissue and minimize risk of hepatotoxicity

Demonstrated significant anti-tumor activity in animal models of resistant tumors as well as those that progressed on anti-PD-1/L1 treatment

Displayed an excellent safety profile in GLP toxicology studies

ATN-031
Target and Modality
CD24 Monoclonal Antibody
Rationale
CD24 is a cell surface protein implicated in tumor cell proliferation and immune evasion. By targeting CD24 with a monoclonal antibody, this asset aims to disrupt the immunosuppressive signaling and enhance immune-mediated tumor cell killing through macrophage-dependent tumor cell phagocytosis
Differentiation

First in class target

No clinical competitor

Showed mono-therapy in vivo efficacy and synergy with chemotherapy, rituximab and CPI

ATN-022
Target and Modality
Claudin 18.2 ADC
Rationale
Claudin 18.2 is a tumor-specific antigen overexpressed in various solid tumors, making it an ideal target for an antibody-drug conjugate. By selectively delivering a cytotoxic payload to tumor cells expressing Claudin 18.2, this asset aims to minimize systemic toxicity while maximizing anti-tumor efficacy
Differentiation

High affinity antibody (pM); Strong in vivo efficacy pre-clinically in Claudin 18.2 low expression PDX models

Demonstrated an excellent safety profile in GLP toxicology studies

ATN-037
Target and Modality
CD73 Small Molecule
Rationale
CD73 is an ecto-enzyme that promotes the production of immunosuppressive adenosine in the tumor microenvironment. Inhibiting CD73 with a small molecule has the potential to reverse an immunosuppressed tumor microenvironment by reducing adenosine-mediated immunosuppression and restore anti-tumor immune responses
Differentiation

Orally bioavailable small molecule that completely overcomes 'hook effect' common in other anti-CD73 antibodies

Tissue penetrance not achievable with mAbs

Promising preclinical efficacy as a monotherapy and strong combination potential

ATN-101
Target and Modality
PD-L1/4-1BB Bispecific Antibody
Rationale
Harnesses the power of immuno-oncology by simultaneously blocking PD-L1, a key immune checkpoint, and conditionally activating the 4-1BB costimulatory receptor on T cells. This dual approach can potentially enhance anti-tumor immune response more effectively than targeting either pathway alone while minimizing risk for 4-1BB related liver toxicity
Differentiation

PD-L1 cross-linking dependent activation of 4-1BB to avoid unwanted 4-1BB signaling in normal tissue and minimize risk of hepatotoxicity

Demonstrated significant anti-tumor activity in animal models of resistant tumors as well as those that progressed on anti-PD-1/L1 treatment

Displayed an excellent safety profile in GLP toxicology studies

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