Privacy Policy

This privacy policy describes the types of personal information collected through NATSARpharmaceuticals.com (“website”) and how NATSAR (“we, our, us”) uses, shares, and protects that information.

Applicability of This Privacy Policy

This privacy policy applies to the personal information NATSAR collects on this website (NATSARpharmaceuticals.com).

Information Visitors Provide to Us

We may collect and store personal information that our website visitors voluntarily provide when they contact us through this website. Personal information may include the visitor’s name, email address, telephone number, or home address. We use this information to respond to visitors' requests and questions.

Cookies

Cookies are bits of text that are placed on a website visitor’s computer hard drive or Internet-connected device. Cookie technology holds information that a site may need to personalize a visitor’s experience. Cookies may also be used for security purposes and to gather statistical data about how visitors navigate and use the website, such as which pages they visit, what they download, and the paths they take to find the website and move from page to page.

NATSAR uses cookies to identify visitors and to track their usage of our website. Visitors who do not wish to have cookies placed on their computers may disable cookies within their browser before using our website.

Sharing Information

We do not sell or otherwise disclose personal information we collect about website visitors, except as described herein or otherwise disclosed to visitors at the time the data are collected.

We may share information provided by our website visitors with service providers we have retained to perform services on our behalf including, without limitation, hosting or operating this website, carrying out visitors’ requests, responding to visitors’ inquiries, and analyzing data. By contract we require these service providers to appropriately safeguard the privacy and security of personal information they process on our behalf.

We may disclose information about a visitor, as compelled or required by law, to law enforcement authorities or other government officials, to protect or defend our legal rights, or to investigate, prevent, or take action regarding illegal activities, suspected fraud, or violations of our terms of use for this website or other applicable policies.

We also reserve the right to transfer personal information we have collected through our website in the event that we sell or transfer all or a portion of our business.

Security

The security of personal information is important to us, and we are committed to using reasonable measures to protect the personal information we may collect. However, due to the inherently open nature of the Internet, we cannot guarantee that communications between our website visitors and us, or the information stored on this website, are absolutely secure.

Links to Other Websites

This website may provide links to other websites for our visitors’ convenience and information. These websites may operate independently from us. NATSAR is not responsible for the privacy or security practices of these sites or content contained therein. We strongly encourage visitors to review these sites to better understand their procedures for collecting, using, and disclosing personal information.

Offline Privacy Policy

This privacy policy applies only to information collected through our website and not to information collected offline.

Children

We do not knowingly collect or solicit personally identifiable information from or about children under the age of 13.

Consent

By using this website, visitors consent to the processing of their personal information as described in this privacy policy.

Changes to This Privacy Policy

We reserve the right to change or add to this privacy policy from time to time and will post any revisions on this website. We will indicate at the bottom of the privacy policy when it was most recently updated. We encourage visitors to check back often to review the latest version.

Questions or Concerns

If you have any questions, concerns, or complaints regarding this privacy policy or privacy issues related to the website, you can contact us at vraman@natsarpharmaceuticals.com

Privacy Policy Effective Date: Sept. 15, 2016

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Terms & Conditions

Introduction

NATSAR provides this website for visitors’ personal informational, educational, and entertainment use. These terms of use governing access to and use of this website should be read carefully before using the website. Within these terms of use, “we” and “our” refer to NATSAR, and “you” and “your” refer to any individual, company, or legal entity that accesses or otherwise uses this website (NATSARpharmaceuticals.com).

Acceptance of the Terms of Use

By using the website, you agree to be legally bound by these terms of use and you agree to the processing of your personal data in accordance with our privacy policy. If you do not agree with these terms of use or our privacy policy, you should not use the website. 

Modifications

These terms of use may be amended by NATSAR, in its sole discretion, at any time without notice to you. Amendments to the terms of use shall be effective upon posting. By continuing to access or use this website, you will be deemed to have accepted such amendments. You are advised to regularly review any applicable terms and conditions. NATSAR reserves the right to discontinue or make changes or updates with respect to the website or its content at any time without notice.

Revisions and Errata

The content appearing on this website may include technical, typographical, or photographic errors. We do not warrant that any of the content on the website is accurate, complete, or current. We may make changes to the website content at any time without notice. We do not, however, make any commitment to update the content.

Your Obligations

NATSAR grants permission to temporarily download the materials (information or software) on this website for personal, noncommercial viewing only. This is the grant of a license, not a transfer of title. Under this license you may not:  

  • Modify or copy the materials.
  • Use the materials for any commercial purpose or for any public display (commercial or noncommercial).
  • Use or access the website for any fraudulent or unlawful purpose.
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  • Attempt to decompile or reverse-engineer any software contained on the website.
  • Restrict or inhibit the ability of any other person to access or use the website.
  • Remove, obscure, or modify any copyright, trademark, or other proprietary notations on the website.

Links

From time to time, the website may include links to third-party websites. These links are provided for your convenience only and do not signify that we endorse such third-party websites. We do not review such third-party websites. In accessing them, you acknowledge and agree that:

  • We are not responsible for such websites, including the terms on which such websites are made available and the privacy policies of such websites, and we do not control their content or availability. 
  • We make no representation, warranty, or condition, either express or implied, in relation to any goods or services or information received from such websites.
  • You access any such website entirely at your own risk.

NATSAR recommends that you make yourself aware of and read the legal and privacy notices of all other websites that you visit. 

Legal Disclaimers

Except as expressly provided in these terms of use, this website is made available to you on an “as is” basis.  We disclaim and do not accept any liability to you with respect to the website, your use of it, or otherwise. It is your responsibility to ensure that the website is suitable for your intended purposes. We make no warranties, expressed or implied, and hereby disclaim and negate all other warranties, including without limitation implied warranties or conditions of merchantability, fitness for a particular purpose, and noninfringement of intellectual property or other violation of rights.

We give no warranty:

  • That access to the website will be uninterrupted or error-free; 
  • That the website and/or the computer server from which the website is made available are free of viruses or other harmful components; or 
  • As to the accuracy, content, timeliness, completeness, reliability, quality, or suitability of any content contained in or delivered via the website or otherwise made available in connection with the website. 

You also acknowledge and agree that the operation of the website is dependent on the proper and effective functioning of the Internet and other third-party equipment and services, and that we do not guarantee and will not be liable for these in any way.

We will not be liable to you for any special, indirect, or consequential losses or damages, or any loss of data, profits, revenues, business, or goodwill. Because some jurisdictions do not allow limitations on implied warranties or limitations of liability for consequential or incidental damages, these limitations may not apply to you.

TO THE MAXIMUM EXTENT PERMITTED BY APPLICABLE LAW, YOU EXPRESSLY WAIVE ALL CLAIMS AGAINST NATSAR AND ITS AFFILIATES AND THEIR OFFICERS, DIRECTORS, EMPLOYEES, SHAREHOLDERS, SUPPLIERS, AND PROGRAMMERS THAT MAY ARISE FROM YOUR ACCESS OR USE OF THIS WEBSITE.

Indemnification and Release

You agree to indemnify, defend, and hold harmless NATSAR and its affiliates against all claims, demands, causes of action, losses, expenses, damages, and costs, including any reasonable attorneys' fees, resulting or arising from or relating to:

  • Your use of or conduct on the website
  • Any activity related to use of the website by you
  • Any message or material that you submit to, post on, or transmit through the website
  • Your violation of these terms of use
  • Your infringement or violation of any rights of another
  • Termination of your access to the website

If you have a dispute with one or more users, you release NATSAR and its affiliates from claims, demands, or damages (actual and consequential) of every kind and nature, known and unknown, arising out of or in any way connected with such disputes.

Intellectual Property Rights

The intellectual property rights in this website and copyright in all material stored, displayed, and accessible on the website are either owned by us or duly licensed by third parties. All such rights are reserved.

Governing Law

These terms of use and any dispute or claim arising out of or in connection with these terms of use or their subject matter (including noncontractual disputes or claims) are subject to the laws of the State of Maryland without regard to its conflict of law provisions.

Severability

If any provision of these terms of use is held to be unlawful, void, or for any reason unenforceable by a court of competent jurisdiction, then the invalid or unenforceable provision shall be replaced by a valid, enforceable provision that most closely matches the intent of the original provision, and the validity and enforceability of any remaining provisions shall not be affected. 

No Waiver

The failure of NATSAR and its affiliates to enforce any part of these terms of use shall not constitute a waiver of such term or provision, and shall not be considered a waiver or limit of NATSAR’s right thereafter to insist on strict adherence to that term or any other provision of these terms of use. 

Terms of Use Effective Date: Sept. 15, 2016

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Research and Development that creates hope. Natsar is developing innovative therapies that could deliver profound impact in fighting lung, brain & breast cancer, sarcoma, and many other diseases.

Learn More About Us

Who is Natsar?

Natsar Pharmaceuticals is an applied research and drug development company focused on the development of novel treatments for cancer and other diseases. In our quest to characterize cellular pathways that are essential for the oncogenic state, we have focused on helicases which are dysregulated in many cancer types.

One such helicase is DDX3, which is overexpressed in many cancer types and has been associated with lower survival in lung cancer patients. We have synthesized a DDX3 inhibitor, RK‐33, which can potentially be used in cancer treatment. Binding of RK‐33 to DDX3 impedes the function of DDX3, resulting in activation of cell death pathways, inhibition of the Wnt‐signaling pathway, and abrogation of non‐homologous end‐joining (NHEJ) activity. In combination with radiation, synergistic cell death effects have been observed both in vitro and in multiple preclinical cancer models. We are currently moving this synthesized compound into clinical trials.

Leadership
Scientific Advisory Board
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Venu Raman Ph.D

Professor, Johns Hopkins University, Founder & Director, NATSAR

Venu Raman, Ph.D, Chief Scientific Officer

Dr. Venu Raman is a Professor in the Johns Hopkins Medicine Department of Radiology and Radiological Science and Department of Oncology and Director of Molecular Therapeutics-Division of Cancer Imaging. His research focuses on developmental cancer biology. Dr. Raman’s work on deciphering the role of HOXA5 and Twist in breast cancer formation is widely recognized both nationally and internationally. He is affiliated with the John Hopkins Medicine In vivo Cellular Molecular Imaging Center.

His current research integrates molecular and cellular biology, developmental biology, cancer biology, molecular imaging and targeted drug development. He is leading research projects that determine the role of dysregulated genes in cancer, and the translatability of this information to a clinical setting. In this regards, he has done extensive research on deciphering the functional role of a RNA helicase gene, DDX3 in biogenesis of multiple cancer types such as breast, lung, sarcoma, colorectal and prostate. Using rational drug design approach, a small molecule inhibitor of DDX3 (RK-33) was synthesized, which provided Dr. Raman with a tool to not only understand the biology of DDX3 but to use it as a targeted therapy for cancer treatment.

Dr. Raman received his undergraduate degree in microbiology from the University of Bombay and his masters of microbiology from the University of Baroda. He earned his Ph.D. in molecular and developmental biology from the University of New South Wales. He completed a postdoctoral fellowship at The Institute of Molecular and Cellular Biology from Indiana University and followed that with a research fellowship at The Johns Hopkins University. Dr. Raman joined the Johns Hopkins faculty in 2000.

Dr. Raman serves on the editorial board of Molecular Medicine Reports and Molecular Cancer Biology. He has been awarded several patents for his research and inventions related to cancer biology.

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David Loeb M.D.,Ph.D

ACTING CHIEF CLINICAL OFFICER

David Loeb M.D.,Ph.D, Chief Clinical Officer

Dr. Loeb is a Professor and Chair of the Department of Pediatrics, Division of Pediatric Hematology and Oncology at Albert Einstein College of Medicine. Prior to taking up this position, he was an Associate Professor of Oncology and Pediatrics and Director of the Musculoskeletal Tumor Program at Johns Hopkins School of Medicine. He has broad expertise in cancer and its treatment, including acute lymphoblastic leukemia (ALL), acute myeloid leukemia, aplastic anemia, bone marrow transplant, bone tumors, chronic myeloid leukemia, clinical trials, Ewing's sarcoma, graft-versus-host disease, hematologic malignancies, Hodgkin's disease, leukemia, leukemia/lymphoma, myelodysplastic syndromes (MDS), non-Hodgkin's lymphoma, osteosarcoma, rhabdomyosarcoma, soft tissue sarcoma, and soft tissue tumors.

His research interests revolve around translational research related to childhood sarcomas. He has a laboratory research effort aimed at understanding the role of a transcription factor called WT1 in the biology of sarcomas, and his work has been instrumental in demonstrating the importance of the RNA helicase DDX3 for Ewing sarcoma. His laboratory is conducting preclinical research on a number of compounds that show scientific promise for the treatment of sarcomas, and he is involved in numerous clinical trials, both investigator-initiated trials at Johns Hopkins as well as trials run through cooperative groups.

Dr. Loeb received his undergraduate degree in biology from Johns Hopkins University in 1987. He earned is PhD from Columbia University in 1993 and an MD from Columbia University in 1994. He completed an internship and residency in Pediatrics at Johns Hopkins University between 1994 and1997 and then a fellowship in pediatric hematology/oncology between 1997 and 2000. He has been a member of the faculty at Johns Hopkins University since 2000.

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Phuoc Tran M.D.,Ph.D

Phuoc Tran M.D.,Ph.D

Dr. Phuoc T. Tran is the Clinical Director of Radiation Oncology, Professor of Radiation Oncology and Molecular Radiation Sciences, Oncology and Urology at the Sidney Kimmel Comprehensive Cancer Center at the Johns Hopkins Hospital and treats patients with cancers of the genitourinary system and uses stereotactic radiation techniques (such as SRS and SBRT/SABR) for the treatment of patients with oligometastatic disease. His research focuses on the improvement of clinical radiotherapy for the treatment of primarily prostate cancer, but also adrenal, bladder, urethral, testicular and penile cancer as well as patients with oligometastatic disease.

Dr. Tran completed his medical and graduate training at the Oregon Health & Sciences University in Portland. He conducted a residency in radiation oncology at the Stanford University School of Medicine in 2008 where he was an instructor of radiation oncology before then joining the staff of Johns Hopkins.

Dr. Tran has published more than 60 scholarly works, has received numerous awards for his research, and is a primary investigator on a number of clinical trials. He is a member and holds leadership positions in the Radiological Society of North America (RSNA) and the American Society for Radiology Oncology (ASTRO), and is board certified in radiation oncology by the American Board of Radiology.

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Paul van Diest M.D.,Ph.D

Paul J van Diest M.D.,Ph.D

Paul J van Diest studied Medicine, did his PhD and pathology residency at the VU University medical center (VUMC) in Amsterdam. After obtaining his Board certification in Pathology in 1996, he became Consultant Pathologist at the Department of Pathology of the VUMC. In 1999 he was appointed Associate Professor and in 2001 to full Professor. In 2003 he moved to Utrecht to become Head of the Department of Pathology at the University Medical Center Utrecht (UMCU) where he is currently still working. He is Adjunct Professor of Oncology at the Sidney Kimmel Oncology Center at Johns Hopkins, Baltimore, USA, and visiting professor at the University of Siena in Italy. He serves on the editorial board of 23 international journals, and is academic editor of PlosOne, BMC Cancer and Pathology Research International. He has been active in the board as secretary and president of several international societies (ESACP, ISCO, ISDQP), and is a board member of the Netherlands Society of Oncology. He is an active cancer researcher with focus on breast carcinogenesis and progression and digital pathology, has published >600 papers in peer reviewed journals, personally supervised 60 PhD theses, and has an H-index of 65.

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Vered Stearns M.D.

Vered Stearns, M.D.

Dr. Vered Stearns completed a B.S. equivalent at the Tel Aviv University, Sackler Faculty of Medicine in 1989. After relocating to the United States, Dr. Stearns transferred to and graduated from the University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School in 1992. She completed a residency in Internal Medicine and a fellowship in Medical Oncology at the Georgetown University where she developed an interest in translational breast cancer research and spent two additional years as a research fellow. Dr. Stearns was a faculty member at the Lombardi Comprehensive Cancer Center and the Georgetown University, and at the University of Michigan Comprehensive Cancer Center in Ann Arbor, Michigan before joining the faculty at the Breast Cancer Program at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins in 2002. She has since been appointed as co-Director of the Breast Cancer Program in 2010, and to full Professor in 2013. In 2014 she was appointed at the co-Director of the Breast and Ovarian Cancer Program at The Kimmel Cancer Center at Johns Hopkins.

Dr. Stearns’s long-term research goal is to improve current therapies by individualizing strategies for the treatment and prevention of breast cancer. Her main research includes utilization of biomarkers to predict response to standard regimens used to treat and prevent breast cancer and to introduce new treatments. While administering standard chemotherapy in the preoperative setting, Dr. Stearns examines molecular markers and functional imaging to assist in the early determination of sensitivity or resistance to different treatments. Dr. Stearns and colleagues from the Consortium On Breast Cancer Pharamcogenomics (COBRA) Group were the first to evaluate the role of genetic variants in candidate genes such as CYP2D6 in tamoxifen metabolism, safety, and efficacy. The work has been extended to evaluate the role of genetic variants in aromatase inhibitor associated outcomes.

Dr. Stearns has received numerous grants and awards to fund her innovative research. She is an Editorial Board Member Clinical Cancer Research, Breast Cancer Research and Treatment, and ONCOLOGY. Dr. Stearns’s work has been presented in key national meetings, and has been published in high-impact peer-reviewed journals. Her work has been cited extensively and has already had a positive impact on the lives of many women.

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Yoon-Jae Cho M.D.

Yoon-Jae Cho, M.D.

Dr. Yoon-Jae Cho, MD is the Ericksen Family Endowed Professor for Research and Chief of the Division of Pediatric Neurology at the Oregon Health & Science University.  Prior to moving to Oregon, he held faculty positions at Harvard Medical School then Stanford University School of Medicine.  Dr. Cho's lab has published seminal work on the genomic characterization of the childhood brain tumor medulloblastoma, the most common malignant brain tumor in children.  His lab discovered the high prevalence of DDX3 mutations in medulloblastoma and were the first published large scale analysis of RNAs bound by DDX3.  In addition to his bench research, Dr. Cho has chaired committees in the Pediatric Brain Tumor Consortium (PBTC) and Children’s Oncology Group (COG), leading the design and execution of several early phase clinical trials.

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The Technology

Based on our identification of an RNA helicase, DDX3, which is overexpressed in many cancer types and has been associated with lower survival in lung cancer patients, we have designed a first‐in‐class small molecule inhibitor, RK‐33, which binds to DDX3 and abrogates its activity. Inhibition of DDX3 by RK‐33 causes G1 cell cycle arrest, induces apoptosis, and promotes radiation sensitization in DDX3‐overexpressing cells. Overall, inhibition of DDX3 by RK‐33 promotes tumor regression, thus providing a compelling argument to develop DDX3 inhibitors for cancer therapy.

The Target

DDX3 is a member of the DEAD‐box family which is involved in a number of cellular processes such as transcription, RNA splicing, mRNA export, and translation initiation (Lorsch, 2002; Rocak & Linder, 2004). DDX3 has also been associated with cancer biogenesis (Hu et al, 2004). We identified DDX3 in a microarray screen of breast cancer cells exposed to cigarette smoke and demonstrated its role in cancer progression (Botlagunta et al, 2008).

DDX3 promotes proliferation and cellular transformation (Hu et al, 2004; Shih et al, 2007; Lee et al, 2008), has anti‐apoptotic properties (Li et al, 2006; Sun et al, 2008, 2011), modulates cell adhesion and motility (Chen et al, 2014), and responds to hypoxia via HIF‐1α (Botlagunta et al, 2011; Bol et al, 2013).

Also, recent evidence has identified that DDX3 acts as an allosteric activator of casein kinase 1 in the Wnt/β‐catenin pathway (Cruciat et al, 2013). Initially, the Wnt/β‐catenin pathway was described in colon cancer. Activating mutations of DDX3 were also shown to be involved in pathogenic Wnt pathway activation in medulloblastoma (Jones et al, 2012; Pugh et al, 2012; Robinson et al, 2012) and chronic lymphatic leukemia (CLL) (Wang et al, 2011). Recently, it has been shown that activated Wnt signaling predicts decreased survival in lung cancer patients (Xu et al, 2011; Shapiro et al, 2013) and decreases sensitivity to radiation therapy (Woodward et al, 2007; Zhang et al, 2010).

The Solution

RK‐33 binds to DDX3 and abrogates its activity, causing G1 cell cycle arrest, inducing apoptosis, and promoting radiation sensitization in DDX3‐overexpressing cells. Mechanistically, loss of DDX3 function either by shRNA or by RK‐33 impaired Wnt signaling through disruption of the DDX3–β‐catenin axis and inhibited non‐homologous end joining—the major DNA repair pathway in mammalian somatic cells. Inhibition of DDX3 by RK‐33 promotes tumor regression, thus providing a compelling argument to develop DDX3 inhibitors for cancer therapy. RK‐33 combined with radiation therapy has been shown to induce tumor regression in lung cancer models, with no toxicity at the therapeutic dose.

Results Include:

  • Knockdown of DDX3 in highly aggressive lung cancer cell lines (H1299 and A549) curbed their colony‐forming abilities.
  • A small molecule inhibitor of DDX3, RK‐33, designed to bind to the nucleotide‐binding site within the DDX3 protein was synthesized.
  • RK‐33 was able to induce cell cycle arrest causing apoptosis in aggressive lung cancer, but not in normal cells, and promoted sensitization to radiation in DDX3‐overexpressing cells. Mechanistically, RK‐33 inhibited non‐homologous end joining and impaired Wnt signaling by disrupting the DDX3–β‐catenin axis.
  • RK-33 displays strong efficacy in multiple solid tumor models including: sarcoma, breast, prostate, colorectal, lung, and medulloblastoma.
  • RK‐33 in combination with radiation, induced tumor regression in multiple mouse models of lung cancer, while showing no toxicity at the therapeutic dose.
  • No observable toxicity in rat blood/liver profiles in both immune competent & immune suppressed mice.
  • Demonstrated RK-33’s effect to preferentially kill cancer cells while sparing normal cells.
  • Generated an antibody that can detect DDX3 in biopsy samples and therefore identify appropriate patients.

Clinical Development

Our clinical development plan will include sarcoma and breast cancer. We will use a novel, biomarker-driven Phase I trial design. Enrollment will be limited to patients with DDX3 expression demonstrated on a pre-treatment tumor biopsy. Dose finding will be based on a Continual Reassessment Model, and there will be a sarcoma-only expansion cohort at the recommended Phase II dose to obtain preliminary evidence of efficacy, increased data on toxicity, and to allow pharmacodynamic and pharmacokinetic studies. Subsequent clinical development is planned in multiple solid tumors including prostate, and medulloblastoma, and in combination with radiation.

News & Press Releases

Read more about Natsar below.

Johns Hopkins Highlights Dr. Venu Raman's Work Developing RK-33Johns Hopkins Highlights Dr. Venu Raman's Work Developing RK-33
December 5, 2023

Dr. Venu Raman is a professor with @Hopkins_Rad and has been developing an exciting drug called RK-33 that is nearing clinical trials and will be a first-in-class cancer treatment with the ability to mitigate many other diseases including SARS-CoV-2 and RSV. #FacultyFriday

Promising Anti-Cancer Drug Also May Function as COVID-19 Antiviral TherapyPromising Anti-Cancer Drug Also May Function as COVID-19 Antiviral Therapy
September 8, 2022

Today's press release by Johns Hopkins Medicine about our work with RK-33.

Natsar's new research "RK-33, a small molecule inhibitor of host RNA helicase DDX3, suppresses multiple variants of SARS-CoV-2" was published today in Frontiers in MicrobiologyNatsar's new research "RK-33, a small molecule inhibitor of host RNA helicase DDX3, suppresses multiple variants of SARS-CoV-2" was published today in Frontiers in Microbiology
August 25, 2022

DDX3 is a host DEAD-box RNA helicase that is usurped by SARS-CoV-2 for virus production.  When the researchers inhibited DDX3 with a small molecule inhibitor, RK-33, viral load was reduced in four isolates of SARS-CoV-2 (including the Delta variant) by one to three log orders in Calu-3 cells.  The data presented supports the use of RK-33 as a host targeting antiviral (HTA) strategy to control SARS-CoV-2 infection, irrespective of its mutational status, in humans.

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Selective cell death in HIV-1-infected cells by DDX3 inhibitors leads to depletion of the inducible reservoirSelective cell death in HIV-1-infected cells by DDX3 inhibitors leads to depletion of the inducible reservoir
May 27, 2021

Target Update - A newly released paper by Rao, et al looked at the impact of DDX3 inhibition on inducing selective cell death in HIV infected cells .  The group demonstrated that Natsar's DDX3 inhibitor, RK-33, was able to bring HIV cells out of latency and induce apoptosis, thereby reducing the total virus reservoir.

The authors conclude, "DDX3 inhibitors are especially interesting as a potential therapeutic class of compounds for use in curative strategies against HIV-1 because they target multiple steps of the HIV-1 life cycle."  

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Study Validates Role of RK-33 to Inhibit SARS-CoV-2 InfectionStudy Validates Role of RK-33 to Inhibit SARS-CoV-2 Infection
April 6, 2021

A recent non-clinical study by Fimia et al. (Proteomic Analysis Identifies the RNA Helicase DDX3 as a Host Target Against SARS-CoV2 Infection) in the journal Antiviral Research adds further support to the role of DDX3 as a host target against SARS-CoV2 infection.  The study also demonstrated that inhibition of DDX3 by RK-33 significantly reduced SARS-CoV-2 replication in cell culture.


New Review Article: Targeting Host DEAD-box RNA Helicase DDX3X for Treating Viral InfectionsNew Review Article: Targeting Host DEAD-box RNA Helicase DDX3X for Treating Viral Infections
January 1, 2021

January 2021 – A new review article “Targeting host DEAD-box RNA helicase DDX3X for treating viral infections” is published in Antiviral Research by Natsar's founder and Professor of Radiology and Oncology at Johns Hopkins School of Medicine, Dr. Venu Raman.  Natsar’s small molecule, RK-33 has been demonstrated to effectively abrogate virion production in both + ssRNA (DENV, WNV, and ZIKA) and -ssRNA (RSV and hPIV-3) infections.

RNA Polymerase II-Associated Factor 1 Regulates Stem Cell Features of Pancreatic Cancer Cells, Independently of the PAF1 Complex, via Interactions with PHF5A and DDX3RNA Polymerase II-Associated Factor 1 Regulates Stem Cell Features of Pancreatic Cancer Cells, Independently of the PAF1 Complex, via Interactions with PHF5A and DDX3
November 1, 2020

In pancreatic CSCs, PAF1 forms a sub-complex that regulates expression of genes that control stem cell features. Knockout of PAF1 reduced the ability of pancreatic tumors to develop and progress in mice and numbers of CSCs.

Target Update: "RNA-binding protein DDX3 mediates posttranscriptional regulation of androgen receptor: A mechanism of castration resistance"Target Update: "RNA-binding protein DDX3 mediates posttranscriptional regulation of androgen receptor: A mechanism of castration resistance"
October 26, 2020

In this paper by Vellky et al. the authors have demonstrated that high DDX3 expression downregulates androgen receptor (AR) expression, leading to the generation of castration-resistant prostate cancer phenotypes. Interestingly, the authors showed that treatment with RK-33, both in vitro and in vivo, deregulates DDX3 expression, thus sensitizing the castration-resistant prostate cancer cells to AR-signaling inhibitors. Significance of this finding is that use of RK-33, in a clinical setting, for castration-resistant prostate cancer treatment is a strategy that can be exploited both to decrease the generation of castration-resistant prostate cancers as well as potentially prevent the recurrence of castration-resistant prostate cancer.

Natsar releases new podcast, “Cancer Matters with Dr. Bill Nelson – Developing a Cancer Drug”.Natsar releases new podcast, “Cancer Matters with Dr. Bill Nelson – Developing a Cancer Drug”.
February 3, 2020

In this week's Cancer Matters podcast, Dr. Bill Nelson speaks with Dr. Venu Raman about his work to develop a cancer drug targeting a gene that stabilizes tumors.

Bringing Johns Hopkins’ Discoveries to the WorldBringing Johns Hopkins’ Discoveries to the World
November 15, 2019
Targeting RNA Helicase DDX3 in Stem Cell Maintenance and Teratoma FormationTargeting RNA Helicase DDX3 in Stem Cell Maintenance and Teratoma Formation
January 25, 2019
RK-33 - Hopkins MedicineRK-33 - Hopkins Medicine
May 3, 2018

Raman’s drug discovery began with research to understand the effect of secondhand smoke on breast cancer. It led him and his team to develop a first in-class drug called RK-33. Countless hours in the lab and hundreds of experiments and assays later, Raman and his team have developed and patented a small molecule inhibitor of the DDX3 gene, an exciting first-in-class pharmaceutical.

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