Our programs 1
Phase 1
Phase 2
Phase 3
Anti-Galectin-9 MAb
Solid tumors and hematological malignancies


Solid tumors

>32K/year U.S. (Metastatic pancreatic cancer)
>33K/year U.S. (Metastatic CRC)
>4K/year U.S. (Metastatic cholangiocarcinoma)

Fully human monoclonal antibody designed to inhibit the activity of galectin-9, a key molecule expressed by tumors and immune cells and shown to suppress the immune system from recognizing and destroying cancer cells, which we are developing for difficult-to-treat cancer indications with poor survival rates, including pancreatic ductal adenocarcinoma (PDAC), colorectal cancer (CRC) and cholangiocarcinoma (CCA).

Phase completedPhase in progress

1 We have an active IND on file with the FDA for LYT-200. The FDA and corresponding regulatory authorities will ultimately review our clinical results and determine whether our wholly-owned therapeutic candidates are safe and effective. No regulatory agency has made any such determination that LYT-200 is safe or effective for use by the general public for any indication.

Monoclonal antibody targeting galectin-9 in development for the potential treatment of solid tumors 

LYT-200 is a fully human IgG4 monoclonal antibody, or mAb, designed to inhibit the activity of galectin-9, a key molecule expressed by tumors and immune cells and shown to suppress the immune system from recognizing and destroying cancer cells. We are developing LYT-200 for difficult-to-treat cancer indications, including pancreatic ductal adenocarcinoma (PDAC), colorectal cancer (CRC) and cholangiocarcinoma (CCA).

  • Key Points of Innovation & Differentiation
    • Immune checkpoint inhibitors, including therapies that target programmed cell death protein 1, or PD-1, programmed death ligand 1, or PDL-1, and cytotoxic T-lymphocyte-associated antigen 4, or CTLA-4, have been developed to counteract multiple mechanisms of immune evasion by a number of different tumor types. Recent reports suggest that marketed drugs against these targets had sales exceeding $28 billion in 20202. Unfortunately, a large proportion of patients, especially those with immunologically silent tumors such as PDAC, CCA and some types of CRC respond sub-optimally to such agents.
    • Galectin-9 promotes and facilitates multiple immunosuppressive pathways by, for example, expanding regulatory T cells, shifting macrophages from the M1 to M2 phenotype, and inducing apoptosis of activated CD4+ and CD8+ T cells. High expression of galectin-9 is evident in tumors and in cancer patients’ blood and correlates with poor survival outcomes and aggressive disease in multiple solid tumor types. We are advancing LYT-200 to inhibit the multiple effects of galectin-9 and thereby potentially removing a key immunosuppressive barrier that would enable the immune system to attack and destroy the tumor.


    • A 2021 study published in Nature Communications proposed that the molecular mechanism by which PD-1 and galectin-9 interact to shield tumors from the immune system demonstrates for the first time that galectin-9 is a ligand for PD-1 and emphasizes its importance as a promising target for immunotherapy3. The work revealed that PD-1 physically interacts with galectin-9 and TIM-3 to attenuate galectin-9/TIM-3-induced T cell apoptosis and maintain effector T cells in the tumor microenvironment in an exhausted functional state. It also showed that interferons significantly upregulate galectin-9 expression and secretion in both immune and cancer cells. Overall, the work provided further evidence that galectin-9 acts as a key regulator of the immune response to tumors and supports its importance as a potential target for cancer treatment.
    • Under normal physiological conditions, galectin-9 is expressed at low levels, which supports the potential safety of LYT-200 in clinical settings. Lack of toxicity/tolerability issues to date in our good laboratory practice (GLP) studies with LYT-200 – even at extremely high doses, such as 300 mg/kg in non-human primates (~100 mg/kg human equivalent dose) – further supports this view.
    • We are not aware of any other clinical development program targeting galectin-9 as a therapeutic target, and thus, we believe that LYT-200 may represent the most advanced clinical program against this target. None of the other human galectins have been documented to play such a global role as galectin-9 in immunosuppression in the context of cancer. We also believe that LYT-200 has the potential to be used as a single agent and safely in combination with checkpoint inhibitors and other chemotherapeutics, depending on the cancer. Additionally, we believe that targeting galectin-9 gives LYT-200 the potential to address a high unmet need for more effective and less toxic therapies for acute myeloid leukemia (AML), a devastating disease in which prognosis is poor, with a roughly 30% five-year survival rate.
  • Program Discovery Process by the PureTech Team
    • In order to identify approaches with the potential to provide significant therapeutic benefit to cancer patients, we undertook a global, proactive search to identify therapeutic targets that mediate multiple mechanisms of immunosuppression. Through our extensive network of advisors and collaborators, we identified a foundational immunosuppressive mechanism involving galectin-9, the therapeutic target of LYT-200, which was the basis of certain intellectual property that we licensed from New York University prior to publication in Nature Medicine 5.
  • Patient Need & Market Potential
    • In the U.S., there are approximately 62,210 new pancreatic cancer patients, of which 52% present with metastatic disease, approximately 151,030 new CRC patients, of which 22% present with metastatic disease, and approximately 8,000 new CCA patients, of which 50% present with metastatic disease, in each case, per year. Unfortunately, a large proportion of patients, especially those with immunologically silent tumors such as PDAC, CCA and some types of CRC respond sub-optimally to immune checkpoint inhibitors, representing a significant patient population that has yet to receive benefit from any immunotherapy agents.
  • Milestones Achieved & Development Status
    • Clinical program
      • In December 2022, we announced that a poster presentation describing the new preclinical data supporting the clinical potential of LYT-200 for the treatment of leukemia was given at the American Society of Hematology (ASH) 64th Annual Meeting. In all models used, LYT-200 demonstrated significant anti-tumor activity and in addition to its established effects on the immune system in solid tumor models, it also notably induced direct apoptosis or cell death across all leukemia cell types. In a model assessing DNA damage in AML cells, LYT-200 significantly outperformed an anti-TIM3 antibody and had effects that were comparable to Venetoclax, an approved therapeutic for AML. The effects were greatest when both compounds were combined. The in vitro efficacy of LYT-200 against the leukemia subtypes also extended to in vivo survival benefit in both immunocompromised and immunocompetent patient-derived xenograft mouse models. In these models, LYT-200 outperformed chemotherapy and produced the greatest effect in combination. Based on this and other compelling preclinical data generated with LYT-200 in blood cancers, we initiated a clinical trial to evaluate LYT-200 as a single agent for the treatment of AML.
      • In December 2022, we also announced the results fromcompletion of the bi-monthly and weekly, monotherapy dose escalation portion of the Phase 1 program assessing the safety and tolerability of escalating doses of LYT-200 as a potential treatment of metastatic solid tumors. the Phase 1/2 clinical trial evaluating LYT-200 in single agent cohorts. No dose-limiting toxicities were reported, and the full results will be presented in an upcoming scientific forum.
      • In November 2021, the FDA granted orphan drug designation to LYT-200 for the treatment of pancreatic cancer. The FDA grants orphan drug designation to novel drug and biologic products for the treatment, diagnosis or prevention of conditions affecting fewer than 200,000 persons in the U.S. Orphan drug designation qualifies PureTech for incentives under the Orphan Drug Act, including tax credits for some clinical trials and eligibility for seven years of market exclusivity in the U.S. if the drug is approved, in addition to our broad intellectual property coverage which can extend the exclusivity into 2038.
      • In November 2021, we announced that a poster presentation describing the adaptive Phase 1/2 trial of LYT-200 for the potential treatment of difficult-to-treat solid tumors was given at the Society for Immunotherapy of Cancer (SITC) 36th annual meeting.
      • In July 2021, we announced a clinical trial and supply agreement with an affiliate of BeiGene, Ltd. to evaluate BeiGene's tislelizumab, an anti-PD-1 monoclonal antibody, in combination with LYT-200. Under the terms of the agreement, we will maintain control of the LYT-200 program, including global R&D and commercial rights. BeiGene has agreed to supply tislelizumab for use in combination with LYT-200 for the planned Phase 2 study cohorts.
    • Preclinical results
      • LYT-200 has been observed to have high specificity for its primary target galectin-9: This was established using a protein array that assessed binding of LYT-200 to more than 5,000 cell bound and secreted human proteins.
      • LYT-200 blocks the galectin-9-CD206 interaction: LYT-200 is able to block functional activity of galectin-9, including its interactions with a specific binding partner/receptor, e.g., CD206. This was established using an ELISA assay demonstrating a galectin-9/CD206 interaction, which could be inhibited by the addition of LYT-200.
      • LYT-200 protects MOLM-13 T cells from galectin-9-mediated apoptosis: LYT-200 has also been observed to protect T cells from
        apoptosis mediated by galectin-9. For example, galectin-9 was shown to significantly increase apoptotic death of MOLM-13 cells. Treatment with LYT-200 in the presence of galectin-9 significantly reduced the percentage of T cells undergoing apoptosis in a dose dependent manner.
      • LYT-200 exceeded anti-PD-1 activity in the B16F10 melanoma model, a gold standard for measuring checkpoint inhibitor efficacy: To further characterize the potential of LYT-200 as a single agent, we created a mouse isotype of LYT-200 (mIgG1-200). mIgG1 200 (LYT-200 designed for mouse in vivo models) reduced mean tumor weights by approximately 50% while an anti-PD-1 antibody reduced mean tumor weights by approximately 22%, which is what is typically seen in the model. We also observed that when an anti-PD-1 antibody was used in combination with mIgG1-200, the number of tumor-infiltrating cytotoxic T cells detected in tumors approximately doubled. These data demonstrate efficacy of mIgG1-200, both as a single agent and in combination with a checkpoint inhibitor.
      • LYT-200 inhibited tumor growth, induced T cell activation and increased survival in the orthotopic pancreatic cancer KPC model where anti-PD1 agents are ineffective: The orthotopic KPC mouse model is commonly used as a preclinical model for evaluating PDAC biology and therapeutic agent efficacy. Anti-PD-1 checkpoint inhibitors have previously proven ineffective in this syngeneic model. Single agent activity of mIgG1-200 was observed in the KPC mouse pancreatic cancer model as illustrated in the figure below. We have evaluated the combination of mIgG1 200 with the standard of care for pancreatic cancer, (e.g., chemotherapy: gemcitabine/nab-paclitaxel). We observed a clear survival improvement with mIgG1 200, both as a single agent and in combination with clinical standard of care chemotherapy.


      • LYT-200 activates T cells in cultured patient-derived organoid tumors, or PDOTs: One of the major challenges in oncology research is the translation from mouse models to humans, particularly in the case of immuno-oncology. To address this concern, we explored LYT-200 activity in cultured PDOTs that mimic human tumor composition within the context of a tumor microenvironment. The aim of treating PDOTs was to assess the ability of LYT-200 to induce T cell activation, which may predict how LYT-200 would behave in humans. LYT-200 potently and reproducibly activated T cells in 56% of the samples tested (n=23).


      • GLP toxicology studies were carried out in Sprague Dawley rats and cynomolgus monkeys. No safety pharmacology findings that were attributed to LYT-200 at doses as high as 300 mg/kg/week were observed with repeat dose exposure.
  • Expected Milestones
    • The combination part of the Phase 1 trial in certain metastatic solid tumors with LYT-200 in combination with tislelizumab is expected to begin in the first quarter of 2023.
    • Results from the Phase 1b clinical trial to evaluate LYT-200 as a single agent for the treatment of AML are expected in 2023.
  • Intellectual Property
    • We have broad intellectual property coverage for these antibody-based immunotherapy technologies, including exclusive rights to six families of patent filings that are exclusively licensed from or co-owned with New York University which cover antibodies that target galectin-9, including LYT-200, methods of using these antibodies and related immuno-oncology technologies. In addition, the intellectual property portfolio includes three families of PureTech-owned patent applications covering the use of anti-galectin-9 antibodies in the diagnosis and treatment of solid tumors.
    • As of December 31, 2021, there are nine families of intellectual property within this patent portfolio covering compositions of matter for antibodies targeting galectin-9, including LYT-200, and methods of use for the treatment of solid tumors, such as pancreatic cancer, CRC, melanoma, gastric cancer, breast cancer and various other cancers. This intellectual property comprises two issued U.S. patents which are expected to expire in 2038, 10 pending U.S. patent applications, which if issued, are expected to expire 2037-2042, four international PCT applications, twenty-four pending foreign applications and five issued patents in foreign jurisdictions.

2 GlobalData Sales and Forecast Database (2021).

3 Yang, Riyao, et al. “Galectin-9 Interacts with PD-1 and TIM-3 to Regulate T Cell Death and Is a Target for Cancer Immunotherapy.” Nature Communications, 5 Feb. 2021, (preclinical data).

4 Limagne, E., Richard, C., Thibaudin, M., Fumet, J. D., Truntzer, C., Lagrange, A., Favier, L., Coudert, B., & Ghiringhelli, F. (2019). Tim-3/galectin-9 pathway and mMDSC control primary and secondary resistances to PD-1 blockade in lung cancer patients. Oncoimmunology, 8(4), e1564505. (preclinical data).

5 Daley, D., Mani, V., Mohan, N. et al. Dectin 1 activation on macrophages by galectin 9 promotes pancreatic carcinoma and peritumoral immune tolerance. Nat Med 23, 556 – 567 (2017).

6 Analyzed n = 23 tumor samples; Success defined as: >20% upregulation of at last two out of three T cell activation markers; Success achieved in 56% of tumors with majority showing >2 fold activation; Representative data from individual tumors per annotated tumor type are shown.

Our anti-cancer programs target emerging, foundational immunosuppressive mechanisms pursue a differentiated approach to cancer types that currently do not have adequate effective treatments. Given its design to inhibit the activity of galectin-9, LYT-200 is being advanced to potentially remove a key immunosuppressive barrier that would enable the immune system to attack and destroy the tumor. Our fully human monoclonal antibody candidate has potential both as a single agent and in combination with existing therapies such as checkpoint inhibitors and chemotherapeutics.