This is a single-institution, single-arm, open-label Phase 2 trial evaluating evofosfamide in subjects with M1 CRPC who fail first-line ARSIs. In those progressing after second-line Docetaxel or deemed ineligible to it, the use of alternate ARSI remains the most common line of therapy in our Province, in keeping with recent international recommendations. After baseline molecular imaging (PSMA and fluorodeoxyglucose (FDG) PET/CT), prior to evofosfamide initiation, subjects will be encouraged to undergo biopsy of a dominant lesion: FDG-, PSMA-uptake and/or conventional imaging determined (in order, and according to feasibility). Subjects will then receive the alternate ARSI (i.e., different from the one received in first line) as per current standard practice and Provincial drug plan coverage. Additionally, subjects will receive combinatorial evofosfamide at a dose of 480 mg/m2 intravenously (IV) over 60 minutes on Days 1, 8 and 15 of every 28-day cycle. Therapy will continue until disease progression, unacceptable toxicity as a result of evofosfamide, or subject withdrawal. Assessments during evofosfamide treatment will include history, physical exam, and blood tests at each monthly visit to monitor for toxicity. Response and progression will be evaluated by whole-body PSMA PET/CT scan every 8 weeks (± 3 days) and determined using (PE)RECIST v1.1 criteria. PSA, NE markers (e.g., Serum CHGA, NSE), organ function tests (e.g., liver, kidney) and investigational liquid biopsy samples will be followed every cycle (monthly). FDG PET/CT will be performed at baseline, at 6-10 weeks from the date of signing the informed consent form (ICF), and upon progression, irrespective of treatment discontinuation or initiation of another therapy. Subjects will be followed for survival endpoints following completion of this study treatment until death.

Start Date01 Apr 2025

Sponsor / Collaborator

University Health Network

[+1]

NCT06782555

/ RecruitingPhase 1/2

A Phase 1/2 Immunotherapy Study of Evofosfamide in Combination with Zalifrelimab and Balstilimab in Patients with Advanced Solid Malignancies

The purpose of this Phase 1/2 study is to test the overall safety, tolerability, and effectiveness of the combination investigational drugs evofosfamide, zalifrelimab, and balstilimab in treating advanced or metastatic castration-resistant prostate cancer, pancreatic cancer, and human papilloma virus (HPV)-negative squamous cell carcinoma of the head and neck (SCCHN).

Start Date08 Jan 2025

Sponsor / Collaborator

Immunogenesis, Inc.Startup

[+1]

NCT03098160

/ Unknown statusPhase 1

A Phase 1 Immunotherapy Study of Evofosfamide in Combination With Ipilimumab in Patients With Advanced Solid Malignancies

An immunotherapy study combining ipilimumab and evofosfamide for the treatment of patients with confirmed metastatic or locally advanced prostate cancer, metastatic pancreatic cancer, melanoma or human papillomavirus (HPV) negative squamous cell carcinoma of head and neck that have failed to respond to standard therapy, progressed despite standard therapy, for which standard therapy does not offer the potential for increased survival.

Start Date10 May 2017

Sponsor / Collaborator

Threshold Pharmaceuticals, Inc.

[+1]

100 Clinical Results associated with Evofosfamide

100 Translational Medicine associated with Evofosfamide

100 Patents (Medical) associated with Evofosfamide

161

Literatures (Medical) associated with Evofosfamide

06 Jan 2025·JOURNAL OF EXPERIMENTAL MEDICINE

Breathing down resistance: Tackling hypoxia to overcome immunotherapy barriers in lung cancer

Article

Author: Chen, Huanhuan Joyce

In this issue of JEM, Robles-Oteiza et al. (https://doi-org.libproxy1.nus.edu.sg/10.1084/jem.20231106) present compelling evidence linking tumor hypoxia to acquired resistance mechanisms in non-small cell lung cancer (NSCLC) treatments involving immune checkpoint inhibitors (ICIs). Their research advocates targeting these hypoxic tumor regions with hypoxia-activated pro-drugs like TH-302, which may substantially delay the onset of resistance and herald a significant advancement in cancer therapy.

02 Dec 2024·MOLECULAR PHARMACEUTICS

Pathophysiology-Driven Approaches for Overcoming Nanomedicine Resistance in Pancreatic Cancer

Review

Author: Sithara, MS ; Abhi, C ; Mangalanandan, T S ; Nair, Sreejith Thrivikraman ; Kamalasanan, Kaladhar ; Unni, Ashok R. ; Sarma, Manjit ; Pavithran, K.

Tumor heterogeneity poses a significant challenge in cancer therapy. To address this, we analyze pharmacotherapeutic challenges by categorizing them into static and dynamic barriers, reframing these challenges to improve drug delivery, efficacy, and the development of controlled-release nanomedicines (CRNMs). This pathophysiology-driven approach facilitates the design of novel therapeutics tailored to overcome obstacles in pancreatic ductal adenocarcinoma (PDAC) using nanotechnology. Advanced biomaterials in nanodrug delivery systems offer innovative solutions by combining controlled release, stimuli sensitivity, and smart design strategies. CRNMs are engineered to modulate spatiotemporal signaling and control drug release in PDAC, where resistance to conventional therapies is particularly high. This review explores pharmacokinetic considerations for nanomedicine design, RNA interference (RNAi) for stromal modulation, and the development of targeted nanomedicine strategies. Additionally, we highlight the limitations of current animal models in capturing the complexities of PDAC and discuss notable clinical failures, such as PEGylated hyaluronidase (Phase III HALO 109-301 trial) and evofosfamide (TH-302) with gemcitabine (MAESTRO trial), underscoring the need for improved models and treatment strategies. By targeting pathways like Notch and Hedgehog and incorporating stimuli-sensitive and pathway-modulating agents, CRNMs offer a promising avenue to enhance drug penetration and efficacy, reshaping the paradigm of pancreatic cancer treatment.

01 Sep 2024·FREE RADICAL BIOLOGY AND MEDICINE

Pharmacologic ascorbate induces transient hypoxia sensitizing pancreatic ductal adenocarcinoma to a hypoxia activated prodrug

Article

Author: Yamamoto, Kazutoshi ; Krishna, Murali C ; Yasunori, Otowa ; Brender, Jeffrey R ; Crooks, Daniel R ; Kota, Yamashita ; Linehan, W Marston ; Kishimoto, Shun ; Levine, Mark

Hypoxic tumor microenvironments pose a significant challenge in cancer treatment. Hypoxia-activated prodrugs like evofosfamide aim to specifically target and eliminate these resistant cells. However, their effectiveness is often limited by reoxygenation after cell death. We hypothesized that ascorbate's pro-oxidant properties could be harnessed to induce transient hypoxia, enhancing the efficacy of evofosfamide by overcoming reoxygenation. To test this hypothesis, we investigated the sensitivity of MIA Paca-2 and A549 cancer cells to ascorbate in vitro and in vivo. Ascorbate induced a cytotoxic effect at 5 mM that could be alleviated by endogenous administration of catalase, suggesting a role for hydrogen peroxide in its cytotoxic mechanism. In vitro, Seahorse experiments indicated that the generation of hydrogen peroxide consumes oxygen, which is offset at later time points by a reduction in oxygen consumption due to hydrogen peroxide's cytotoxic effect. In vivo, photoacoustic imaging showed pharmacologic ascorbate treatment at sublethal levels triggered a complex, multi-phasic response in tumor oxygenation across both cell lines. Initially, ascorbate generated transient hypoxia within minutes through hydrogen peroxide production, via reactions that consume oxygen. This initial hypoxic phase peaked at around 150 s and then gradually subsided. However, at longer time scales (approximately 300 s) a vasodilation effect triggered by ascorbate resulted in increased blood flow and subsequent reoxygenation. Combining sublethal levels of i. p. Ascorbate with evofosfamide significantly prolonged tumor doubling time in MIA Paca-2 and A549 xenografts compared to either treatment alone. This improvement, however, was only observed in a subpopulation of tumors, highlighting the complexity of the oxygenation response.

News (Medical) associated with Evofosfamide

06 Mar 2025

·www.prnewswire.com

ImmunoGenesis Doses First Patient in Phase 1/2 Clinical Trial of IMGS-101 in Combination With Balstilimab (anti-PD-1) and Zalifrelimab (anti-CTLA-4) in Relapsed or Refractory Advanced Prostate, Pancreatic, and HPV(-) Head & Neck Tumors

IMGS-101 is the only known reducer of solid tumor hypoxia, offering the potential to enhance the efficacy of immunotherapy HOUSTON, March 6, 2025 /PRNewswire/ -- ImmunoGenesis, a clinical-stage biotech company developing innovative, science-driven immunotherapies, today announced the first patient has been dosed in the company's Phase 1/2 clinical trial of its hypoxia reversal agent IMGS-101 (evofosfamide) in combination with Balstilimab (anti-PD-1) and Zalifrelimab (anti-CTLA-4) at The University of Texas MD Anderson Cancer Center in Houston, Texas. Tumor hypoxia (low oxygen levels) is an immunosuppressive factor in solid tumors. By reversing hypoxia, IMGS-101 may improve the efficacy of immunotherapies in cancer types that are otherwise resistant to immune-based treatments. Continue Reading ImmunoGenesis The Phase 1/2, open-label, multicenter study (NCT06782555) consists of a dose escalation and expansion portion to evaluate the safety, pharmacokinetics, and anti-tumor activity of IMGS-101 in combination with Balstilimab and Zalifrelimab in adult patients with locally advanced or metastatic castration-resistant prostate cancer (CRPC), pancreatic cancer, and human papillomavirus-(HPV) negative squamous cell carcinoma of the head and neck (SCCHN). The study is being conducted in collaboration with Agenus, a clinical-stage immuno-oncology company developing the checkpoint inhibitors Balstilimab and Zalifrelimab. "Launching this trial represents a significant milestone in our mission to target key mechanisms of immune resistance," said ImmunoGenesis President and CEO James Barlow. "By targeting and reversing hypoxia, we aim to unlock the immune system's full potential and redefine the therapeutic landscape for these cancers with high unmet medical needs." "This trial marks an exciting step forward in addressing one of the key challenges in cancer immunotherapy," said Dr. Charles Schweizer, Senior Vice President of Clinical Development at ImmunoGenesis. "Hypoxia limits T-cell infiltration and suppresses immune responses, especially in prostate, pancreatic, and head and neck cancers. By reversing hypoxia, IMGS-101 may restore T-cell access to tumors, enhancing the effectiveness of checkpoint inhibitors and potentially transforming outcomes in these hard-to-treat cancers." About ImmunoGenesis ImmunoGenesis is a clinical-stage biotech company dedicated to transforming immuno-oncology by targeting key mechanisms of immune resistance. The company's lead product, IMGS-001, is a cytotoxic, dual-specific PD-L1/PD-L2 antibody currently in a phase 1a/b clinical trial for the treatment of immune-excluded ("cold") tumors, which account for more than half of all cancers. In addition to its lead program, the company is developing a number of novel approaches to overcome immune resistance in cold tumors. ImmunoGenesis designs therapies to address the pathology of these tumors, overcoming immune exclusion to elicit a robust immune response. For more information, visit . About IMGS-101 IMGS-101, also known as Evofosfamide, is a 2-nitroimidazole prodrug of the cytotoxin bromo-isophosphoramide mustard (Br-IPM) originally developed as a hypoxia-activated prodrug. ImmunoGenesis' Founder, Dr. Michael A. Curran from MD Anderson, demonstrated in his lab that IMGS-101 has the unique ability to address one of the most significant immunosuppressive barriers by reversing hypoxia. In pre-clinical models and a Phase 1 clinical study, IMGS-101 restored T-cell function and showed early signs of synergizing with checkpoint inhibitors. ImmunoGenesis is developing IMGS-101 as a hypoxia-reversal agent that can condition tumors to respond to checkpoint inhibition. About Balstilimab Balstilimab is a novel, fully human monoclonal immunoglobulin G4 (IgG4) designed to block PD-1 (programmed cell death protein 1) from interacting with its ligands PD-L1 and PD-L2. It has been evaluated in >900 patients to date and has demonstrated clinical activity and a favorable tolerability profile in several tumor types. Balstilimab is being developed by Agenus, Inc. About Zalifrelimab Zalifrelimab is a novel, fully human monoclonal immunoglobulin G1 (IgG1) designed to block CTLA-4 (cytotoxic T-lymphocyte associated antigen 4) from interacting with its ligands CD80 and CD86. CTLA-4 is a negative regulator of immune activation that is considered a foundational target within the immuno-oncology market. Zalifrelimab is being developed by Agenus, Inc. Disclosure Dr. Curran's financial relationship with ImmunoGenesis is managed and monitored by the MD Anderson Conflict of Interest Committee. Contact ImmunoGenesis Investors: James Barlow President and CEO [email protected] SOURCE Immunogenesis Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

ImmunotherapyPhase 1Clinical Result

13 Feb 2024

·www.globenewswire.com

RAPT Therapeutics Bolsters Leadership Team with the Appointment of Nipun Davar, Ph.D., as Senior Vice President of Technical Operations

SOUTH SAN FRANCISCO, Calif., Feb. 13, 2024 (GLOBE NEWSWIRE) -- RAPT Therapeutics, Inc. (Nasdaq: RAPT), a clinical-stage, immunology-based therapeutics company focused on discovering, developing and commercializing oral small molecule therapies for patients with significant unmet needs in inflammatory diseases and oncology, today announced the appointment of Nipun Davar, Ph.D., as Senior Vice President of Technical Operations. “I am delighted to announce the addition of Nipun to the RAPT leadership team and welcome his wealth of experience in small molecule product development and commercial manufacturing,” said Brian Wong, M.D., Ph.D., President and Chief Executive Officer of RAPT Therapeutics. “Nipun fills an important role as we advance zelnecirnon in late-stage clinical trials for inflammatory diseases and tivumecirnon in oncology indications, executing on our mission to bring promising drug candidates to patients with high unmet needs." Nipun brings over 27 years of extensive biopharmaceutical and drug development experience specializing in successful product development and commercial manufacturing. Most recently he served as Chief Corporate Officer at Astex Pharmaceuticals, Inc., where he oversaw the CMC, program management, legal and finance functions. Prior to Astex Pharmaceuticals, Inc., Nipun was Senior Vice President of Pharmaceutical Development and Manufacturing at Threshold Pharmaceuticals where he led the development of TH-302, a hypoxia activated prodrug developed to treat to multiple cancer types. Earlier in his career, Nipun held various roles encompassing drug delivery-based product development, clinical and commercial supply chain management, regulatory filings and product approvals. Nipun holds a Ph.D. in Pharmaceutical Sciences from the University of Maryland and an MBA from the Wharton School of Business. Nipun added, "I am pleased to join the RAPT leadership team during this exciting period. The company boasts a distinctive and diverse portfolio featuring two internally discovered compounds. Both zelnecirnon and tivumecirnon have demonstrated clinical proof of concept in their respective therapeutic areas, underlining the vast potential to make a positive impact for patients in both inflammatory diseases and oncology. I look forward to contributing to the continued advancement of these promising programs." About RAPT Therapeutics, Inc.RAPT Therapeutics is a clinical-stage, immunology-based therapeutics company focused on discovering, developing and commercializing oral small molecule therapies for patients with significant unmet needs in inflammatory diseases and oncology. Utilizing its proprietary discovery and development engine, the Company is developing highly selective small molecules designed to modulate the critical immune drivers underlying these diseases. RAPT has discovered and advanced two unique drug candidates, zelnecirnon (RPT193) and tivumecirnon (FLX475), each targeting C-C motif chemokine receptor 4 (CCR4), for the treatment of inflammation and cancer, respectively. The Company is also pursuing a range of targets that are in the discovery stage of development. Investor Contact:Sylvia Wheelerswheeler@wheelhouselsa.com Media Contact:Aljanae Reynoldsareynolds@wheelhouselsa.com

Executive Change

03 Nov 2022

·www.prnewswire.com

ImmunoGenesis to Present Pre-Clinical Data from Lead Program at Society for Immunotherapy of Cancer Conference

HOUSTON, Nov. 3, 2022 /PRNewswire/ -- ImmunoGenesis, a clinical-stage biotechnology company developing science-driven immune therapies, today announced that two poster presentations on its lead development program, IMGS-001, will be presented at the Society for Immunotherapy of Cancer 37th Annual Meeting (SITC 2022), November 8-12, 2022, in Boston, MA. The posters will be available on the ImmunoGenesis website following the conference. Poster Presentation Details Development of IMGS-001, a novel anti-PD-L1/PD-L2 dual specific, multi-functional antibody, to treat immune excluded tumors Poster Number: 1333 November 10, 2022 Preclinical characterization of IMGS-001, a dual antagonist anti-PD-L1, anti-PD-L2 antibody with effector function, to treat patients resistant to immune checkpoint blockade Poster Number: 1378 November 11, 2022 About IMGS-001, a PD-L1/PD-L2 Dual-Specific Inhibitor ImmunoGenesis' lead program is IMGS-001, a PD-L1/PD-L2 dual-specific inhibitor with an engineered cytotoxic effector function. As the first molecule to target PD-L2 in addition to PD-L1, IMGS-001 has the potential to shut down the entire PD-1 pathway, potentially providing superior blockade compared to other PD-1 or PD-L1 inhibitors. The built-in engineered effector function allows IMGS-001 to kill immunosuppressive cells that express PD-L1 and/or PD-L2. Preclinical data showed that IMGS-001 offered five times the response rate in cold tumors than currently available immunotherapies. Additionally, IMGS-001 can provide a foundation for add-on therapies. About ImmunoGenesis ImmunoGenesis, Inc., is a clinical stage immuno-oncology biopharmaceutical company re-envisioning "cold" tumor treatment. Representing more than half of all cancers, cold tumors lack activated T cells or have other immune resistance mechanisms, and current immunotherapies have shown limited to no efficacy. ImmunoGenesis' immune therapies are based in the pathology of these cold tumors, transforming them into hot tumors by targeting key mechanisms of immune resistance. For more information about the company, visit . Forward-Looking Statements This press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, included in this press release are forward-looking statements. These forward-looking statements may be identified by terms such as "will," "could," "believe," "plan," "expect," "target," "continue," "to," and similar terms or expressions or the negative thereof. Examples of such statements include, but are not limited to, statements regarding the development and/or effectiveness of evofosfamide and the ability of evofosfamide to achieve the desired results whether as a monotherapy or in combination with other therapies. We may not actually achieve the plans, carry out the intentions or meet the expectations or objectives disclosed in the forward-looking statements. You should not place undue reliance on these forward-looking statements. These statements are subject to risks and uncertainties which could cause actual results and performance to differ materially from those discussed in the forward-looking statements. The forward-looking statements contained in this press release speak only as of the date of this press release and are based on management's assumptions and estimates as of such date. We disclaim any intent or obligation to update these forward-looking statements to reflect events or circumstances that exist after the date on which they were made. Contact Jennifer Guinan Sage Strategic Marketing 610-410-8111 [email protected] SOURCE ImmunoGenesis

CollaborateAntibodyImmunotherapy

100 Deals associated with Evofosfamide

External Link

KEGG	Wiki	ATC	Drug Bank
D10704	Evofosfamide	-	DB06091

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Pancreatic carcinoma non-resectable	Phase 3	US	Threshold Pharmaceuticals, Inc.	01 Dec 2012
Pancreatic carcinoma non-resectable	Phase 3	DE	Threshold Pharmaceuticals, Inc.	01 Dec 2012
Metastatic Soft Tissue Sarcoma	Phase 3	US	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	AT	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	BE	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	CA	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	DK	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	FR	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	DE	Threshold Pharmaceuticals, Inc.	01 Sep 2011
Metastatic Soft Tissue Sarcoma	Phase 3	HU	Threshold Pharmaceuticals, Inc.	01 Sep 2011

Clinical Result

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03098160 (Pubmed \| Clin Cancer Res) Manual	Phase 1	Neoplasms	21	Ipilimumab+Evofosfamide	zfbyusgibb(zgrrkogoif) = yzqmuoecaf cvsnyapcxx (ocabjphqix ) View more	Positive	01 Jun 2021
Pubmed \| Sci Rep Manual	Phase 2	Recurrent Glioblastoma	33	evofosfamide+Bevacizumab	hbshyhxwch(wuozkwfzou) = biiifhsepn pvzqkrffgv (bgvtafwpoi ) View more	Positive	27 Jan 2021
NCT02342379 (CTgov)	Phase 2	Glioblastoma	35	TH-302+Bevacizumab	zietxinpvp(yszqrnhehf) = ukejruhzxf rlxvdfqsyo (dhhspddxtt, vpdhiatnua - qsqxopumno) View more	-	10 Apr 2020
NCT03098160 (P348, SITC2019)	Phase 1	Advanced Malignant Solid Neoplasm	21	Evofosfamide 400mg/m2 + Ipilimumab 3mg/kg	bfgjifdpnt(gbpdoumztz) = n=16 qmprgvmgqn (kayqevhhej ) View more	Positive	01 Nov 2019
NCT03098160 (P348, SITC2019)	Phase 1	Advanced Malignant Solid Neoplasm	21	Evofosfamide 480mg/m2 + Ipilimumab 3mg/kg		Positive	01 Nov 2019
EUCTR2014-004072-30-ES (SUNEVO, ESMO2019)	Phase 2	Pancreatic neuroendocrine tumour metastatic	17	Sunitinib + Evofosfamide	wqnlkfgzvw(sxyaqyimjg) = lnqxhiheuk fqmmasawdd (ryzfznccgx ) View more	-	30 Sep 2019
NCT01403610 (AT-12, CTgov)	Phase 2	Astrocytoma \| High grade glioma	28	Placebo+TH-302 preoperative+bevacizumab 10mg/kg (Cohort 1)	gzaqhbsqqq(dxlvmilckl) = jylgifrvwh guixulvsxe (ykacbdczuo, kovyoqfqnk - vwxxixbywm) View more	-	24 Jul 2019
NCT01403610 (AT-12, CTgov)	Phase 2	Astrocytoma \| High grade glioma	28	TH-302 preoperative+bevacizumab 10mg/kg (Cohort 2)	gzaqhbsqqq(dxlvmilckl) = nufytginbd guixulvsxe (ykacbdczuo, biceyqlkus - mnmkszdipl) View more	-	24 Jul 2019
NCT01522872 (Pubmed) Manual	Phase 1/2	Multiple Myeloma	59	dexamethasone+evofosfamide	kqonphdllw(hszxpegwaw) = gqtdpjhjqq xwujmkrgbl (bmtrhrpkcy ) View more	Positive	15 Jan 2019
NCT01522872 (Pubmed) Manual	Phase 1/2	Multiple Myeloma	59	dexamethasone+bortezomib+evofosfamide	fpfrfghemh(bvnjqxihlh) = jbzxfvbvhd sdqqbnpgtb (updwjplpqe ) View more	Positive	15 Jan 2019
NCT02255110 (CTgov)	Phase 2	Metastatic Soft Tissue Sarcoma	6	TH-302+doxorubicin	xeabcqobdy(usslmkaivo) = yrxoerqvba lvuycnepnw (ytrmpzzfzj, nmhrojvrpm - otlugyswqe) View more	-	14 Dec 2018
NCT01833546 (CTgov)	Phase 1	Solid tumor \| Pancreatic Cancer	20	Evofosfamide (Evofosfamide 240 mg)	yonmvvasqd(trrhzjsqwu) = hmkeknptja jhlmbmvtaw (rlqrmprykl, gsihduvzwx - nthbtyalwe) View more	-	15 Oct 2018
NCT01833546 (CTgov)	Phase 1	Solid tumor \| Pancreatic Cancer	20	Evofosfamide (Evofosfamide 340 mg)	yonmvvasqd(trrhzjsqwu) = wmbvkfsuuu jhlmbmvtaw (rlqrmprykl, vvdbvzklxt - onahmmwyfl) View more	-	15 Oct 2018
NCT02047500 (CTgov)	Phase 1	Pancreatic Cancer	19	TH-302+nab-paclitaxel+Gemcitabine	iwaamkboye(bedlzjalmv) = yjbcjktpcd yxsuziafrc (wzhaipequx, uxztyjtmuj - wvncwzxipl) View more	-	15 Dec 2017

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