The purpose of this study is to evaluate the use of IRX5183 in 1) patients with relapsed and/or refractory AML and 2) patients with high-risk MDS or chronic myelomonocytic leukemia (CMML).

Start Date30 Jan 2017

Sponsor / Collaborator

The Sidney Kimmel Comprehensive Cancer Center

[+1]

NCT02991651 / SuspendedPhase 1

A Phase I Study of IRX4204 in Combination With Erlotinib in Patients With Previously Treated Advanced Non-Small Cell Lung Cancer

Patient selection: a) Pathological confirmation of non-small cell lung cancer without activating EGFR mutations; b) Advanced stage disease (IV or IIIB with malignant effusion) with at least two prior chemotherapy regimens; c) No available curative therapy; d) Pregnant women are excluded; e) Informed consent.
Pretreatment evaluation: a) Medical history and physical examination; b) Hepatic and renal function (bilirubin, aspartate aminotransaminase, creatinine); c) Preoperative staging evaluation including CT-chest or PET/CT scan;
Treatment plan: Three dose levels of IRX4204 and erlotinib will be studied using intra-patient dose escalation for dose levels 1 and 2. These study agents will be administered orally until progression of disease, unacceptable toxicities, activation of a phase II study of the combination, or exhaustion of the IRX4204 drug supply.
Evaluation on study: Adverse events will be graded on a scale of 0 to 5, using the Common Terminology Criteria for Adverse Events (CTCAE) v. 4.0. Efficacy will be assessed using the RECIST v1.1 criteria based on CT-chest or PET/CT scan after 8 weeks of study treatment.

Start Date01 May 2016

Sponsor / Collaborator

Io Therapeutics, Inc.

[+1]

NCT02438215 / CompletedPhase 1

An Open-Label, Single Site Study Using [123I]β-CIT Single Photon Emission Tomography (SPECT) to Evaluate Dopamine Transporter Binding Following Treatment With IRX4204 in Early Parkinson's Disease Subjects

This is a single site, open-label study designed to examine dopamine transporter density using [123I]β-CIT SPECT imaging before and following treatment with IRX4204 for a 30-day period in early Parkinson's disease patients. In addition, clinical evaluations will be performed to evaluate the effect of IRX4204 treatment on the motor and cognitive symptoms of PD.

Start Date01 Aug 2014

Sponsor / Collaborator

Io Therapeutics, Inc.

100 Clinical Results associated with Io Therapeutics, Inc.

0 Patents (Medical) associated with Io Therapeutics, Inc.

Literatures (Medical) associated with Io Therapeutics, Inc.

03 Jun 2024·Clinical Cancer Research

IRX4204 Induces Senescence and Cell Death in HER2-positive Breast Cancer and Synergizes with Anti-HER2 Therapy

Article

Author: Coleman, Darian ; Vuligonda, Vidyasagar ; Lanier, Amanda ; Hill, Jamal ; Mazumdar, Abhijit ; Brown, Powel H. ; Sanders, Martin E. ; Moyer, Cassandra L. ; Qian, Jing

AbstractPurpose:Rexinoids, agonists of nuclear retinoid X receptor (RXR), have been used for the treatment of cancers and are well tolerated in both animals and humans. However, the usefulness of rexinoids in treatment of breast cancer remains unknown. This study examines the efficacy of IRX4204, a highly specific rexinoid, in breast cancer cell lines and preclinical models to identify a biomarker for response and potential mechanism of action.Experimental Design:IRX4204 effects on breast cancer cell growth and viability were determined using cell lines, syngeneic mouse models, and primary patient-derived xenograft (PDX) tumors. In vitro assays of cell cycle, apoptosis, senescence, and lipid metabolism were used to uncover a potential mechanism of action. Standard anti-HER2 therapies were screened in combination with IRX4204 on a panel of breast cancer cell lines to determine drug synergy.Results:IRX4204 significantly inhibits the growth of HER2-positive breast cancer cell lines, including trastuzumab and lapatinib–resistant JIMT-1 and HCC1954. Treatment with IRX4204 reduced tumor growth rate in the MMTV-ErbB2 mouse and HER2-positive PDX model by 49% and 44%, respectively. Mechanistic studies revealed IRX4204 modulates lipid metabolism and induces senescence of HER2-positive cells. In addition, IRX4204 demonstrates additivity and synergy with HER2-targeted mAbs, tyrosine kinase inhibitors, and antibody–drug conjugates.Conclusions:These findings identify HER2 as a biomarker for IRX4204 treatment response and demonstrate a novel use of RXR agonists to synergize with current anti-HER2 therapies. Furthermore, our results suggest that RXR agonists can be useful for the treatment of anti-HER2 resistant and metastatic HER2-positive breast cancer.

02 May 2024·Cancer Research

Abstract PO5-24-12: IRX5010, a Highly Selective RARγ Nuclear Receptor Agonist Compound Inhibits In Vivo Growth of Murine EMT-6 Triple Negative Breast Cancer and Human JIMT-1Her2+ Breast Cancer By Induction of Tumor-Infiltrating Effector Memory T-cells

Author: Vuligonda, Vidyasagar ; Sanders, Martin ; Topalovski, Mary

AbstractResearch Objectives and Rationale: Previously, RARγ agonism has been shown to play an essential role in CD8 T-cell-mediated immunity to infectious pathogens. However, we found no previous reports on effects of RARγ agonists on in vivo tumor growth of triple negative or Her2+ breast cancers. Here we explored whether RARγ could play a critical role in T-cell-mediated immunity in these breast cancers, using potent highly selective novel RARγ agonist compounds.Experimental methods and results: We synthesized and screened compounds for selective transactivation of RAR γ in reporter assays. Three highly potent compounds, demonstrating highly selective RARγ transactivation at less than one nanomolar concentrations, were selected for further evaluation of potential anti-cancer activities in vitro. None of the three evaluated compounds demonstrated significant inhibitory effects on in vitro growth of EMT-6 triple negative breast cancer cells at concentrations of 20-100 millimolar, indicating that the three compounds have insignificant direct inhibitory effects on EMT-6 cancer cell growth in vitro. We then examined the effects of one of the compounds in vivo in a syngeneic mouse model of EMT-6 triple negative breast cancer. Treatment with the most potent of the three compounds, IRX5010, demonstrated dose response inhibition of in vivo growth of EMT-6 tumors. Inhibition of tumor growth at day 17 relative to vehicle was 59% and 69% respectively in mice treated with IRX5010 at 10 or 25 mg/kg/day. A cohort treated with 50 mg/kg/day was sacrificed early on day 12 due to excessive weight loss and deaths of some of the animals. This cohort experienced a 73% inhibition of tumor growth relative to vehicle. Gross necropsies of animals in the 25 and 50 mg/kg/day dose groups did not show observable pathologic findings in any major organ. Flow cytometry was performed on freshly excised tumors on the day of termination of the in-life portion of the study in the 10 and 25 mg/kg/day dose groups. Tumors from mice treated with IRX5010 had increased intratumoral numbers of Total CD45+ cells; Total CD3+, Total CD4+, and Total CD8+ T-cells per mg of tumor tissue, relative to vehicle controls. IRX5010 treated mice also had increased intratumoral CD4+IL-17+ T-helper cells; and increased CD4+CD62L- and CD8+CD62L- T-effector memory T-cells per mg of tumor tissue relative to vehicle-treated control mice.We also conducted an experiment of treatment with IRX5010 in mice transplanted with human immune cells (to provide a human immune system) to examine its effects on xenografted human Her2+ JIMT-1 cancer cells. In this model, treatment with IRX5010 at 10 mg/kg/day resulted in a 17% inhibition of tumor growth relative to vehicle control over 26 days of treatment. Flow cytometric analysis showed that tumors from the IRX5010 treated mice contained increased numbers per mg of tumor tissue of intratumoral human CD8+ T-cells, most of which were CD8+ CD7- CD45RA+ terminally differentiated effector memory phenotype T-cells.Conclusions: Treatment with IRX5010, a potent and highly selective RARγ nuclear receptor agonist compound demonstrated substantial treatment effects relative to vehicle control on inhibition of growth of murine triple negative breast cancer in vivo, despite having essentially no growth inhibitory effect on these cells in vitro. Treatment of xenografted human Her2+ tumors in mice with humanized immune systems resulted in a moderate inhibition of Her2+ breast cancer growth relative to vehicle controls. In both models, treatment with IRX5010 induced tumor infiltrating T-lymphocytes of largely effector memory phenotypes, demonstrating an effect on the tumor immune microenvironment. These data identify RARγ and RARγ agonists as a new treatment target and novel treatment modality for breast cancers, especially for the highly unmet need for new and better treatments for triple negative breast cancer.Citation Format: Martin Sanders, Mary Topalovski, Vidyasagar Vuligonda. IRX5010, a Highly Selective RARγ Nuclear Receptor Agonist Compound Inhibits In Vivo Growth of Murine EMT-6 Triple Negative Breast Cancer and Human JIMT-1Her2+ Breast Cancer By Induction of Tumor-Infiltrating Effector Memory T-cells [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-24-12.

02 May 2024·Cancer Research

Abstract PS07-07: The RXR agonist, IRX4204, delays the formation of Brca1 mutant mammary tumors via modulation of the anti-tumor immune response

Author: Mohammed, Altaf ; Moyer, Cassandra ; Vornik, Lana A. ; Savage, Michelle ; Coleman, Darian ; Shizuko, Sei ; Mazumdar, Abhijit ; Hill, Jamal ; Brown, Powel ; Sanders, Martin

AbstractBackground:Women with germline BRCA1 mutations are at an increased risk for developing breast cancer in their lifetime, often at a young age with more aggressive tumors. At present, prophylactic bilateral mastectomy is the most effective strategy for reducing breast cancer risk. However, this invasive procedure is irreversible and associated with potential complications. We and others have found that PARP inhibitors can delay Brca1-mutant tumor formation in mice and could be beneficial for the prevention of breast cancer. However, currently available PARP inhibitors are associated with modest toxicities that may not be acceptable to women without cancer. Thus, there remains an urgent need for the development of safe and effective therapies for the prevention of breast cancer. Here, we present data demonstrating the activity of IRX4204, a minimally toxic and highly specific agonist of the nuclear retinoid X receptor (RXR), to delay the formation of mammary tumors in a Brca1-deficient mouse model. This inhibitory effect on tumor growth is due, in part, to the role of IRX4204 in stimulating the anti-tumor immune response.Methods:We used the established MMTV-Cre, conditional Brca1 gene knockout, p53 heterozygous loss mouse model (BRCA1co/co; MMTV-Cre+/+; p53+/-) and selected for mutant female pups using PCR genotyping. At 16 weeks of age, all mice were separated into 4 treatment groups (n=10 per group): (1) sesame oil control; (2) the novel RXR agonist, IRX-4204 (10mg/kg); (3) high-dose IRX4204 (20 mg/kg); and (4) the RXR agonist, 9-cis-UAB-30 (5 mg/kg). All treatments were given by oral gavage five days per week, and mice were observed daily for tumor formation and toxicity. At the study endpoint, tumors and normal mammary glands were collected for additional analyses. Immunohistochemical staining was used to quantify CD8a, Ki-67 and cleaved caspase 3 expression in Brca1-deficient tumors. Oil Red O staining was used to measure changes in lipid accumulation in Brca1-deficient cell lines treated with IRX4204. qPCR was used to quantify the changes in gene expression of lipid metabolism-associated genes upon treatment with IRX4204 in vitro.Results:Vehicle-treated Brca1-deficient mice had a median time-to-tumor formation (TTF) of 211 days, with 100% developing tumors by 330 days. Mice treated with UAB 5 mg/kg had an improved median TTF of 261 days, whereas mice treated with IRX4204 10mg/kg or 20mg/kg had a median TTF of 347 and 304 days, respectively (p < 0.01). In addition, 60% of mice treated with IRX4204 10 mg/kg remained tumor-free at 330 days. IRX4204-treated tumors showed an increased infiltration of CD8-positive T-cells over vehicle-treated tumors (p < 0.05). Treatment of Brca1-deficient cell lines with IRX4204 in vitro resulted in a significant increase in lipid accumulation accompanied by a 2-fold increase of Srebf1 expression (a key transcription factor that regulates lipid homeostasis) within 24 hours of treatment (p < 0.05).Conclusion:These data demonstrate a novel use of the RXR agonist, IRX4204, to delay the formation of Brca1-deficient mammary tumors. We have found that IRX4204 treatment modulates the tumor immune response through increased infiltration of cytotoxic CD8-positive T-cells in Brca1-deficient mammary tumors in vivo. We have also determined that IRX4204 modulates lipid metabolism in breast cancer cell lines in vitro. It is known that lipid-derived antigens can stimulate T-cell activity. Our findings suggest that RXR agonists may alter lipid antigen production to activate an anti-tumor response. Additional immune and lipidomic studies are on-going. This work was supported by NCI-PREVENT grant (to PB and AM HHSN26100008) and CFP Foundation (Odyssey Fellowship to CM).Citation Format: Cassandra Moyer, Darian Coleman, Jamal Hill, Lana A. Vornik, Michelle Savage, Martin Sanders, Sei Shizuko, Altaf Mohammed, Powel Brown, Abhijit Mazumdar. The RXR agonist, IRX4204, delays the formation of Brca1 mutant mammary tumors via modulation of the anti-tumor immune response [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PS07-07.

News (Medical) associated with Io Therapeutics, Inc.

08 Jul 2024

·www.biospace.com

Io Therapeutics, Inc., announces presentation of data on induction of tumor growth inhibiting anti-cancer immune responses in multiple types of cancers by a IRX5010, a novel retinoic acid nuclear receptor agonist compound

SPRING, Texas, July 08, 2024 (GLOBE NEWSWIRE) --Io Therapeutics Inc., presented today results from studies done in breast, lung, colorectal, and prostate cancer models with the company’s newest anti-cancer compound IRX5010, an agonist of retinoic acid nuclear receptor gamma which was discovered in the company’s oncology drug program. The presentation titled “RAR Gamma Agonist Compounds Promote Effector Memory Tumor Infiltrating T-cells and are Effective in Multiple Cancer Models”, which was delivered at the Federation of American Societies for Experimental Biology (FASEB) Seventh International Conference on Retinoids, being held in St. Paul, Minnesota, USA; was authored by Vidyasagar Vuligonda, Ph.D., Chief Science Officer of the company and inventor of the compound; and Martin E. Sanders, M.D., the company’s Chief Executive Officer. The presented studies showed that oral treatment with IRX5010 resulted in suppression of growth in mouse models of each of five types of the most prevalent and deadly cancers in humans, i.e. triple negative breast, Her-2 positive breast, non-small cell lung, colorectal, and prostate cancers. In all five models, treatment with IRX5010 induced tumor infiltrating effector memory phenotype T-lymphocytes associated with reduction in tumor growth. Treatment with IRX5010 did not directly impact growth of cancers cells in tissue cultures, indicating that the compound is not significantly directly toxic to cancer cells. The data support that the compound’s mechanism of anti-tumor activity is induction of cancer suppressive tumor-infiltrating T-lymphocytes, so called TILs, rather than direct toxic effects on the cancer cells. Orally administered drugs which induce TILs as a mechanism of action for treatment of cancers are being widely sought in the pharmaceutical industry. Dr. Vuligonda stated, “These results disclose a new approach to potentially improving treatment of multiple types of serious cancers in humans using IRX5010 as monotherapy, or potentially in combination with other agents such as biologic checkpoint inhibitors, which also induce anti-cancer TIL responses. We are currently conducting preclinical combination studies of IRX5010 with other agents. We anticipate advancing IRX5010 as monotherapy, and as combination therapy other already available treatments, into clinical trials in multiple types of cancers.” Dr. Sanders stated, “IRX5010 has potential to be a new effective oral immunotherapeutic treatment for many types of currently inadequately treated human cancers, including the most common types of mortal cancers. In addition to IRX5010, Io Therapeutics has discovered multiple families of compounds targeting other retinoic acid nuclear receptors, which the company is developing as potential treatments for cancers, neurodegenerative, and autoimmune diseases.” About Io Therapeutics: Io Therapeutics, Inc. is a privately held company headquartered in Spring, Texas. More information on Io Therapeutics and its product development programs is available on the company’s web site: Forward Looking Statements: This new release contains "forward-looking statements" within the meaning of the safe harbor provisions of the United States Private Securities Litigation Reform Act of 1995. Contact: info@io-therapeutics.com

AACRImmunotherapy

21 Mar 2024

·www.prnewswire.com

Immuno-Oncology Therapies: In-Depth Analysis of the Rapidly Evolving Landscape in Next-Generation Cancer Treatment

DUBLIN , March 20, 2024 /PRNewswire/ -- The "Innovation Waves in Immuno-oncology Therapy Development" report has been added to ResearchAndMarkets.com's offering. Immuno-oncology (I-O) therapies target tumors by harnessing the host's immune system. With the growing incidence and prevalence of various types of aggressive and refractory cancers, the next-generation I-O therapy pipeline has witnessed significant growth. Chimeric antigen receptor (CAR)-T cell therapy and tumor-targeted antibody therapies, including monoclonals, antibody-drug conjugates (ADCs), bispecific antibodies, and several therapeutic cancer vaccines, are making rapid strides in clinical trials as effective immunotherapy. This study discusses the key trends and technologies driving the development of such I-O therapies. It delves into advancements in cancer vaccines and cell therapies for various cancer indications, highlighting some of the innovators in this space. Next-generation cell therapies, personalized cancer vaccines, and strategic areas of focus have also been discussed in this report. The study examines the factors driving and restraining this industry and identifies the growth opportunities emerging from the changes in this space for market players and stakeholders to leverage. Key questions answered in this study: What does the current clinical landscape of I-O therapies look like? Which are the technology enablers driving the adoption of I-O therapies? What are the key developments in adoptive cell therapies and cancer vaccines? What are the roadblocks to successful translation? What are the research and development (R&D) focus areas? What are the key focus areas for the future? Key Growth Opportunities Growth Opportunity 1: Combination Immunotherapies Growth Opportunity 2: Precision Oncology Growth Opportunity 3: Advanced Synthetic Biology Platforms Growth Opportunity 4: Organoids and Organ-on-Chip Models Key Topics Covered: Growth Environment: I-O Therapies Need for Immunotherapy Scope of Analysis Segmentation: Snapshot of I-O Therapies I-O Therapies in Development Growth Opportunities in I-O Therapy Growth Drivers Growth Restraints Trends and R&D Focus: I-O Therapies I-O Technology Trends and Developments Trends in I-O Therapeutics Therapeutic Development Trends in I-O R&D Focus Areas to Boost Immunotherapies Modulation of TME: Solid Tumor Type Determines Therapy Developing Effective Preclinical Models for Translation Stakeholders Developing Preclinical Models for I-O Therapy Evaluation Holistic Tumor Profiling to Boost Precision Oncology Efforts Emerging I-O Therapeutic Modality Development Landscape Quick Facts on I-O Therapies Clinical Development Landscape of I-O Therapies Cell Therapy to Create the Next Wave of I-O Developments Cell Therapy Types: Snapshot Clinical Development Landscape of I-O Cell Therapies Emerging Areas of Focus to Improve Functionality and Safety Cell Therapies Next-generation CAR-T Therapy Development Priority Areas to Improve the Accessibility of Cell Immunotherapy Innovative Technologies for Cell Therapy Manufacturing and Delivery Stakeholders Developing Emerging Next-gen Cell Therapies Potential of Vaccines to Address Challenges with Difficult-to-Treat Cancers Cancer Vaccine Types Personalized Neoantigen Vaccines in Clinical Development Areas of Focus to Bolster Cancer Vaccine Development RNA Vaccines to Drive the Wave of Prophylactic and Therapeutic Cancer Vaccines Road Ahead for Cancer Vaccines and Immunotherapy Emerging Cancer Vaccine Impact of Emerging Cancer Vaccines Across Cancers I-O Stakeholder Ecosystem Regional Trends in I-O Developments and Adoption Federal Initiatives and Programs Driving I-O Therapy Development I-O Deals and Investment Trends Notable Partnerships and Collaborations in I-O, 2023 I-O Regulatory Environment and Reimbursement I-O: Current Gaps and Potential Opportunities Strategies to Improve Access and Care Delivery of I-O Therapies For more information about this report visit About ResearchAndMarkets.com ResearchAndMarkets.com is the world's leading source for international market research reports and market data. We provide you with the latest data on international and regional markets, key industries, the top companies, new products and the latest trends. Media Contact: Research and Markets Laura Wood, Senior Manager [email protected] For E.S.T Office Hours Call +1-917-300-0470 For U.S./CAN Toll Free Call +1-800-526-8630 For GMT Office Hours Call +353-1-416-8900 U.S. Fax: 646-607-1907 Fax (outside U.S.): +353-1-481-1716 Logo: SOURCE Research and Markets

ImmunotherapyVaccineCell TherapyASCOAACR

12 Sep 2023

·www.biospace.com

Io Therapeutics, Inc., Announces Publication of Data on a Novel Compound Promoting Anti-Cancer Immune Responses

SPRING, Texas, Sept. 12, 2023 (GLOBE NEWSWIRE) -- Io Therapeutics, Inc., announced today the publication in Scientific Reports – Nature Publishing Group, of results from studies done with the company’s novel anti-cancer compound IRX4647, an agonist of the retinoic acid nuclear receptor gamma, discovered in the company’s oncology drug program. The paper, titled “A novel retinoic acid receptor-gamma agonist antagonizes immune checkpoint resistance in lung cancers by altering the tumor immune microenvironment,” authored by Cheng-Hsin Wei, Ph.D., et al., reports studies done in the laboratory of the Molecular Pharmacology Program at the Frederick National Laboratory for Cancer Research (FNLCR), supervised by Xi Liu, Ph.D., Senior Principal Scientist; and Ethan Dmitrovsky, M.D., president of Leidos Biomedical Research and Director of the Frederick National Laboratory for Cancer Research. The studies showed that oral treatment with IRX4647 in combination with an immune checkpoint inhibitor (anti-PD-L1) resulted in suppression of a typically checkpoint inhibitor treatment-resistant syngeneic lung cancer in mice. IRX4647 did not appreciably impact growth of the lung tumor cells in cultures, indicating that the compound alone is not directly toxic to lung cancer cells. Studies in other syngeneic mouse cancer models implicated the tumor microenvironment in these anti-cancer effects since T cell depletion antagonized those effects. Notably, treatment of mice with IRX4647 in combination with the checkpoint inhibitor increased the presence of CD-4 T-lymphocytes in the tumors, indicating that the compound’s anti-cancer effects were mediated through promotion of anti-cancer immune responses in combination with the checkpoint inhibitor. Dr. Dmitrovsky stated, “These results reveal an approach to potentially improve treatment of cancers in humans using combinations of retinoic acid nuclear receptor gamma agonists with checkpoint inhibitors. Future clinical trials could address this possibility.” Martin Sanders, M.D., Chief Executive Officer of Io Therapeutics noted that “Scientific Reports – Nature Publishing Group” is the fifth most highly cited scientific journal in the world. “That these results were published so prominently in the literature indicates their importance to the future of cancer therapeutics.” Sagar Vuligonda, Ph.D, Chief Scientific Officer of Io Therapeutics stated “The company has designed, synthesized, and patented multiple structural families of compounds which bind selectively to the retinoic acid nuclear receptor gamma, and to various other retinoic acid nuclear receptor targets, which we are pursuing as potential treatments for diverse cancers, and also for treatment of neurodegenerative and autoimmune diseases such as Parkinson’s disease and psoriasis.” About Io Therapeutics: Io Therapeutics, Inc. is a privately held company headquartered in Spring, Texas, focused on the development of novel retinoic acid-based compounds for treatment of cancers, neurodegenerative diseases, and autoimmune diseases. More information on Io Therapeutics is available on the company’s web site: Forward Looking Statements: This new release contains "forward-looking statements" within the meaning of the safe harbor provisions of the United States Private Securities Litigation Reform Act of 1995. Contact: info@io-therapeutics.com

ImmunotherapyAACR

100 Deals associated with Io Therapeutics, Inc.

100 Translational Medicine associated with Io Therapeutics, Inc.

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Pipeline Snapshot as of 23 Dec 2024

The statistics for drugs in the Pipeline is the current organization and its subsidiaries are counted as organizations,Early Phase 1 is incorporated into Phase 1, Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3

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Drug(Targets)	Indications	Global Highest Phase

IRX-4204 ( RXRs )	Non-Small Cell Lung Cancer More	Phase 2
IRX-5010 ( RARγ )	HER2 Positive Breast Cancer More	Preclinical
IRX-4647 ( RARγ )	Lung Cancer More	Preclinical
VTP-195183 ( RARα )	Refractory acute myeloid leukemia More	Discontinued
IRX-4310 ( RARs )	Neutropenia More	Pending

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