The PTPN2/PTPN1 inhibitor ABBV-CLS-484 unleashes potent anti-tumour immunity

Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance 1 , 2 . The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion...

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Published inNature (London) Vol. 622; no. 7984; pp. 850 - 862
Main Authors Baumgartner, Christina K., Ebrahimi-Nik, Hakimeh, Iracheta-Vellve, Arvin, Hamel, Keith M., Olander, Kira E., Davis, Thomas G. R., McGuire, Kathleen A., Halvorsen, Geoff T., Avila, Omar I., Patel, Chirag H., Kim, Sarah Y., Kammula, Ashwin V., Muscato, Audrey J., Halliwill, Kyle, Geda, Prasanthi, Klinge, Kelly L., Xiong, Zhaoming, Duggan, Ryan, Mu, Liang, Yeary, Mitchell D., Patti, James C., Balon, Tyler M., Mathew, Rebecca, Backus, Carey, Kennedy, Domenick E., Chen, Angeline, Longenecker, Kenton, Klahn, Joseph T., Hrusch, Cara L., Krishnan, Navasona, Hutchins, Charles W., Dunning, Jax P., Bulic, Marinka, Tiwari, Payal, Colvin, Kayla J., Chuong, Cun Lan, Kohnle, Ian C., Rees, Matthew G., Boghossian, Andrew, Ronan, Melissa, Roth, Jennifer A., Wu, Meng-Ju, Suermondt, Juliette S. M. T., Knudsen, Nelson H., Cheruiyot, Collins K., Sen, Debattama R., Griffin, Gabriel K., Golub, Todd R., El-Bardeesy, Nabeel, Decker, Joshua H., Yang, Yi, Guffroy, Magali, Fossey, Stacey, Trusk, Patricia, Sun, Im-Meng, Liu, Yue, Qiu, Wei, Sun, Qi, Paddock, Marcia N., Farney, Elliot P., Matulenko, Mark A., Beauregard, Clay, Frost, Jennifer M., Yates, Kathleen B., Kym, Philip R., Manguso, Robert T.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 26.10.2023
Nature Publishing Group
Subjects
101/58
13/1
13/106
13/21
13/31
13/51
14
14/34
38/39
38/91
42/41
59/5
60 APPLIED LIFE SCIENCES
631/67/1059/2325
631/67/580
64/60
692/308/2778
96/1
96/31
Animal models
Animals
Antibodies
Antigens
Bioavailability
Cancer
Cancer immunotherapy
CD8 antigen
CD8-Positive T-Lymphocytes - drug effects
CD8-Positive T-Lymphocytes - immunology
Cell culture
Cell growth
Clonal deletion
Design
Disease Models, Animal
Drug dosages
Drug Resistance, Neoplasm
Humanities and Social Sciences
Humans
Immune Checkpoint Inhibitors
Immune system
Immunity
Immunotherapy
Immunotherapy - methods
Inhibitors
Interferons - immunology
Killer Cells, Natural - drug effects
Killer Cells, Natural - immunology
Kinases
Lymphocytes
Lymphocytes T
Mice
multidisciplinary
Naphthalenes - pharmacology
Natural killer cells
Neoplasms - drug therapy
Neoplasms - enzymology
Neoplasms - immunology
Patients
PD-1 protein
Phosphatase
Phosphorylation
Plasma
preclinical research
Protein Tyrosine Phosphatase, Non-Receptor Type 1 - antagonists & inhibitors
Protein Tyrosine Phosphatase, Non-Receptor Type 2 - antagonists & inhibitors
Proteins
PTPN2 protein
Science
Science (multidisciplinary)
Signal transduction
Solid tumors
T cell receptors
Therapeutic targets
Thiadiazoles - pharmacology
Tumor microenvironment
Tumor Microenvironment - drug effects
Tumor Microenvironment - immunology
Tumors
tumour immunology
Tyrosine
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Abstract Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance 1 , 2 . The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity 3 – 6 . However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8 + T cell function by enhancing JAK–STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994 ). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes. An orally bioavailable small-molecule active-site inhibitor of the phosphatases PTPN2 and PTPN1, ABBV-CLS-484, demonstrates immunotherapeutic efficacy in mouse models of cancer resistant to PD-1 blockade.
AbstractList Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance1,2. The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity3-6. However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8+ T cell function by enhancing JAK-STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994 ). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes.Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance1,2. The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity3-6. However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8+ T cell function by enhancing JAK-STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994 ). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes.
Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance 1,2 . The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity 3–6 . However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8 + T cell function by enhancing JAK–STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994 ). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes.
Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance. The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity. However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8+ T cell function by enhancing JAK–STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes.
Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance 1 , 2 . The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity 3 – 6 . However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8 + T cell function by enhancing JAK–STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994 ). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes. An orally bioavailable small-molecule active-site inhibitor of the phosphatases PTPN2 and PTPN1, ABBV-CLS-484, demonstrates immunotherapeutic efficacy in mouse models of cancer resistant to PD-1 blockade.
Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to overcome resistance . The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, and their genetic deletion in either tumour cells or immune cells promotes anti-tumour immunity . However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a first-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro amplifies the response to interferon and promotes the activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8 T cell function by enhancing JAK-STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994 ). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes.
Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and newapproaches are needed to overcome resistance12. The protein tyrosine phosphatases PTPN2 and PTPN1 are central regulators of inflammation, andtheirgenetic deletion in eithertumourcellsor immune cells promotes anti-tumour immunity3 6. However, phosphatases are challenging drug targets; in particular, the active site has been considered undruggable. Here we present the discovery and characterization of ABBV-CLS-484 (AC484), a flrst-in-class, orally bioavailable, potent PTPN2 and PTPN1 active-site inhibitor. AC484 treatment in vitro ampliflesthe response to interferon and promotesthe activation and function of several immune cell subsets. In mouse models of cancer resistant to PD-1 blockade, AC484 monotherapy generates potent anti-tumour immunity. We show that AC484 inflames the tumour microenvironment and promotes natural killer cell and CD8+ T cell function by enhancingJAK-STAT signalling and reducing T cell dysfunction. Inhibitors of PTPN2 and PTPN1 offer a promising new strategy for cancer immunotherapy and are currently being evaluated in patients with advanced solid tumours (ClinicalTrials.gov identifier NCT04777994). More broadly, our study shows that small-molecule inhibitors of key intracellular immune regulators can achieve efficacy comparable to or exceeding that of antibody-based immune checkpoint blockade in preclinical models. Finally, to our knowledge, AC484 represents the first active-site phosphatase inhibitor to enter clinical evaluation for cancer immunotherapy and may pave the way for additional therapeutics that target this important class of enzymes.
Author Paddock, Marcia N.
Geda, Prasanthi
Chuong, Cun Lan
Davis, Thomas G. R.
Duggan, Ryan
Frost, Jennifer M.
Rees, Matthew G.
Dunning, Jax P.
Wu, Meng-Ju
Kennedy, Domenick E.
Roth, Jennifer A.
Hrusch, Cara L.
Kohnle, Ian C.
Suermondt, Juliette S. M. T.
Chen, Angeline
Muscato, Audrey J.
Klinge, Kelly L.
McGuire, Kathleen A.
Griffin, Gabriel K.
Cheruiyot, Collins K.
Fossey, Stacey
Sun, Qi
Kim, Sarah Y.
Decker, Joshua H.
Farney, Elliot P.
Yeary, Mitchell D.
Matulenko, Mark A.
Kammula, Ashwin V.
Golub, Todd R.
Baumgartner, Christina K.
El-Bardeesy, Nabeel
Halvorsen, Geoff T.
Ronan, Melissa
Balon, Tyler M.
Krishnan, Navasona
Manguso, Robert T.
Liu, Yue
Olander, Kira E.
Colvin, Kayla J.
Mathew, Rebecca
Backus, Carey
Klahn, Joseph T.
Sen, Debattama R.
Trusk, Patricia
Beauregard, Clay
Iracheta-Vellve, Arvin
Boghossian, Andrew
Longenecker, Kenton
Sun, Im-Meng
Ebrahimi-Nik, Hakimeh
Hutchins, Charles W.
Halliwill, Kyle
Patel, Chirag H.
Mu, Liang
Bulic, Marinka
Guffroy, Magali
Yates, Kathleen B.
Knudsen, Nelson H.
Avila, Omar I.
Hamel, Keith M.
Patti, James C.
Qi
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  givenname: Kathleen B.
  orcidid: 0000-0002-7383-5573
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  fullname: Manguso, Robert T.
  email: rmanguso@mgh.harvard.edu
  organization: Broad Institute of MIT and Harvard, Center for Cancer Research and Department of Medicine, Massachusetts General Hospital
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37794185$$D View this record in MEDLINE/PubMed
https://www.osti.gov/servlets/purl/2470124$$D View this record in Osti.gov
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2023. The Author(s).
Copyright Nature Publishing Group Oct 26, 2023
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D Anz (6575_CR30) 2015; 75
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AM Bolger (6575_CR52) 2014; 30
SL Lambert (6575_CR24) 2022; 45
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37982351 - Immunol Cell Biol. 2024 Jan;102(1):8-11. doi: 10.1111/imcb.12711
37914810 - Nat Rev Drug Discov. 2023 Dec;22(12):951. doi: 10.1038/d41573-023-00178-7
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Snippet Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and new approaches are needed to...
Immune checkpoint blockade is effective for some patients with cancer, but most are refractory to current immunotherapies and newapproaches are needed to...
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60 APPLIED LIFE SCIENCES
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Animal models
Animals
Antibodies
Antigens
Bioavailability
Cancer
Cancer immunotherapy
CD8 antigen
CD8-Positive T-Lymphocytes - drug effects
CD8-Positive T-Lymphocytes - immunology
Cell culture
Cell growth
Clonal deletion
Design
Disease Models, Animal
Drug dosages
Drug Resistance, Neoplasm
Humanities and Social Sciences
Humans
Immune Checkpoint Inhibitors
Immune system
Immunity
Immunotherapy
Immunotherapy - methods
Inhibitors
Interferons - immunology
Killer Cells, Natural - drug effects
Killer Cells, Natural - immunology
Kinases
Lymphocytes
Lymphocytes T
Mice
multidisciplinary
Naphthalenes - pharmacology
Natural killer cells
Neoplasms - drug therapy
Neoplasms - enzymology
Neoplasms - immunology
Patients
PD-1 protein
Phosphatase
Phosphorylation
Plasma
preclinical research
Protein Tyrosine Phosphatase, Non-Receptor Type 1 - antagonists & inhibitors
Protein Tyrosine Phosphatase, Non-Receptor Type 2 - antagonists & inhibitors
Proteins
PTPN2 protein
Science
Science (multidisciplinary)
Signal transduction
Solid tumors
T cell receptors
Therapeutic targets
Thiadiazoles - pharmacology
Tumor microenvironment
Tumor Microenvironment - drug effects
Tumor Microenvironment - immunology
Tumors
tumour immunology
Tyrosine
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