UPCC 10219: Phase II Study Of Stromal Changes Detected By DCE- and DW-MRI In Response To PEGPH20 Combined With Chemotherapy In Subjects With Locally-Advanced Pancreatic Cancer

This research study is being conducted to determine the effects of PEGPH20 plus chemotherapy treatment on the MRI characteristics of locally advanced pancreatic cancer patient tumors. Subjects will received Gemcitabine, Abraxane and PEGPH20.

Start Date01 Jan 2020

Sponsor / Collaborator

Abramson Cancer Center

[+1]

NCT03979066 / TerminatedPhase 2IIT

A Phase 2, Open-Label, Multicenter, Randomized Study Evaluating NEOadjuvant Immunotherapy Based Combinations in Patients With Resectable PANCreatic Ductal Adenocarcinoma

The purpose of this study is to determine if study treatment with atezolizumab and PEGPH20 given before and after surgery, followed by chemotherapy is safe and if it can further increase the immune response against the tumor rather than increase the chance of cure.

Start Date01 Nov 2019

Sponsor / Collaborator

Columbia University

[+2]

NCT03634332 / Unknown statusPhase 2IIT

Phase II Study of PEGPH20 and Pembrolizumab (MK-3475) for Patients With Previously Treated Hyaluronan High (HA-High) Metastatic Pancreatic Ductal Adenocarcinoma

This study is the study of the combination of PEGPH20 and Pembrolizumab (MK-3475) for patients with previously treated Hyaluronan High (HA-high) metastatic pancreatic ductal adenocarcinoma. This study is an interventional, unblinded, open label study. Approximately 35 subjects will be enrolled. The trial will require approximately a total of 18 months, including 12 months for enrollment, with an additional 6 months for patient follow-up, data collection and study closure.
Each subject will participate in the trial from the time the subject signs the Informed Consent Form (ICF) through the final contact. After a screening phase of up to 21 days, eligible subjects will receive PEGPH20 beginning with Cycle 1 Day 1, on Days 1, 8 15 of every 3 week-cycles and pembrolizumab beginning on Cycle 1 Day 1 (2-4 hrs after PEGPH20), every 3-week-cycles.
Treatment with PEGPH20 and pembrolizumab will continue until progressive disease (PD), unacceptable adverse events (AEs), intercurrent illness that prevents further administration of treatment, investigator's decision to withdraw the subject, subject withdraws consent, pregnancy of the subject, noncompliance with trial treatment or procedure requirements, subject receives 35 treatments (approximately 24 months) of pembrolizumab, or administrative reasons requiring cessation of treatment. Subjects who discontinue for reasons other than PD will have post-treatment follow-up for disease status until PD, initiating a non-study cancer treatment, withdrawing consent, or becoming lost to follow-up. All subjects will be followed by telephone for overall survival (OS) until death, withdrawal of consent, or the end of the study.
After the end of treatment, each subject will be followed for 30 days for AE monitoring. Serious adverse events (SAE) and events of clinical interest (ECI) will be collected for 90 days after the end of treatment or for 30 days after the end of treatment if the subject initiates new anticancer therapy, whichever is earlier.

Start Date01 May 2019

Sponsor / Collaborator

Pancreatic Cancer Research Team

[+3]

100 Clinical Results associated with Pegvorhyaluronidase alfa

100 Translational Medicine associated with Pegvorhyaluronidase alfa

100 Patents (Medical) associated with Pegvorhyaluronidase alfa

Literatures (Medical) associated with Pegvorhyaluronidase alfa

01 Sep 2024·BIOMEDICINE & PHARMACOTHERAPY

Hyaluronidase improves the efficacy of nab-paclitaxel after prolonged angiogenesis inhibition in preclinical models for esophagogastric cancer

Article

Author: Liu, Dajia ; Waasdorp, Cynthia ; Meijer, Sybren L ; Oyarce, Cesar ; Bootsma, Sanne ; Guo, Lihui ; Bijlsma, Maarten F ; van Laarhoven, Hanneke W M

BACKGROUND:

Long-term anti-angiogenesis leads to pruned vasculature, densely deposited extracellular matrix (ECM), and consequently reduced chemotherapy delivery in esophagogastric cancer (EGC). To address this issue, we evaluated the efficacy of adding a hyaluronidase or a NO-donor to the regimen of chemotherapy and anti-angiogenic drugs.

METHODS:

A patient-derived EGC xenograft model was developed. Grafted mice were randomly assigned to four experimental groups and one control group. The experimental groups received DC101, a murine angiogenesis inhibitor, and nab-paclitaxel (NPTX), with the addition of hyaluronidase (PEGPH20), or NO-donor (nitroglycerine, NTG), or their combination, respectively. We compared tumor growth during 17 days of treatment. We performed immunohistochemistry for ECM components hyaluronan (HA) and collagen, CD31 for endothelial cells, and γH2AX for DNA damage. The positively stained areas were quantified, and vessel diameters were measured using QuPath software.

RESULTS:

Prolonged DC101 treatment induced deposition of HA (p<0.01) and collagen (p<0.01). HA was effectively degraded by PEGPH20 (p<0.001), but not by NTG as expected. Both PEGPH20 (p<0.05) and NTG (p<0.01) dilated vessels collapsed in response to long-term DC101 treatment. However, only PEGPH20 (rather than NTG) was found to significantly inhibit tumor growth (p<0.05) in combination with NPTX and DC101.

CONCLUSIONS:

These findings suggest that the mechanical barrier of HA is the major reason responsible for the resistance developed during prolonged anti-angiogenesis in EGC. Incorporating PEGPH20 into the existing treatment regimen is promising to improve outcomes for patients with EGC.

01 Aug 2024·Molecular Metabolism

Limiting extracellular matrix expansion in diet-induced obese mice reduces cardiac insulin resistance and prevents myocardial remodelling

Article

Author: Hasib, Annie ; Wasserman, David H ; Kang, Li ; Musale, Vishal ; Banah, Ayman K ; Hennayake, Chandani K ; Lang, Chim C ; Murdoch, Colin E ; Dong, Bo

OBJECTIVE:

Obesity increases deposition of extracellular matrix (ECM) components of cardiac tissue. Since obesity aggregates with insulin resistance and heart disease, it is imperative to determine whether the increased ECM deposition contributes to this disease cluster. The hypotheses tested in this study were that in cardiac tissue of obese mice i) increased deposition of ECM components (collagens and hyaluronan) contributes to cardiac insulin resistance and that a reduction in these components improves cardiac insulin action and ii) reducing excess collagens and hyaluronan mitigates obesity-associated cardiac dysfunction.

METHODS:

Genetic and pharmacological approaches that manipulated collagen and hyaluronan contents were employed in obese C57BL/6 mice fed a high fat (HF) diet. Cardiac insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp and cardiac function was measured by pressure-volume loop analysis in vivo.

RESULTS:

We demonstrated a tight association between increased ECM deposition with cardiac insulin resistance. Increased collagen deposition by genetic deletion of matrix metalloproteinase 9 (MMP9) exacerbated cardiac insulin resistance and pirfenidone, a clinically available anti-fibrotic medication which inhibits collagen expression, improved cardiac insulin resistance in obese mice. Furthermore, decreased hyaluronan deposition by treatment with PEGylated human recombinant hyaluronidase PH20 (PEGPH20) improved cardiac insulin resistance in obese mice. These relationships corresponded to functional changes in the heart. Both PEGPH20 and pirfenidone treatment in obese mice ameliorated HF diet-induced abnormal myocardial remodelling.

CONCLUSION:

Our results provide important new insights into the role of ECM deposition in the pathogenesis of cardiac insulin resistance and associated dysfunction in obesity of distinct mouse models. These findings support the novel therapeutic potential of targeting early cardiac ECM abnormalities in the prevention and treatment of obesity-related cardiovascular complications.

01 Aug 2023·Molecular imaging and biology

Impact of Arterial Input Function and Pharmacokinetic Models on DCE-MRI Biomarkers for Detection of Vascular Effect Induced by Stroma-Directed Drug in an Orthotopic Mouse Model of Pancreatic Cancer.

Article

Author: Zhou, Rong ; Rosen, Mark ; Cao, Jianbo ; Pickup, Stephen

PURPOSE:

We demonstrated earlier in mouse models of pancreatic ductal adenocarcinoma (PDA) that K^trans derived from dynamic contrast-enhanced (DCE) MRI detected microvascular effect induced by PEGPH20, a hyaluronidase which removes stromal hyaluronan, leading to reduced interstitial fluid pressure in the tumor (Clinical Cancer Res (2019) 25: 2314-2322). How the choice of pharmacokinetic (PK) model and arterial input function (AIF) may impact DCE-derived markers for detecting such an effect is not known.

PROCEDURES:

Retrospective analyses of the DCE-MRI of the orthotopic PDA model are performed to examine the impact of individual versus group AIF combined with Tofts model (TM), extended-Tofts model (ETM), or shutter-speed model (SSM) on the ability to detect the microvascular changes induced by PEGPH20 treatment.

RESULTS:

Individual AIF exhibit a marked difference in peak gadolinium concentration. However, across all three PK models, k_ep values show a significant correlation between individual versus group-AIF (p < 0.01). Regardless individual or group AIF, when k_ep is obtained from fitting the DCE-MRI data using the SSM, k_ep shows a significant increase after PEGPH20 treatment (p < 0.05 compared to the baseline); %change of k_ep from baseline to post-treatment is also significantly different between PEGPH20 versus vehicle group (p < 0.05). In comparison, when k_ep is derived from the TM, only the use of individual AIF leads to a significant increase of k_ep after PEGPH20 treatment, whereas the %change of k_ep is not different between PEGPH20 versus vehicle group. Group AIF but not individual AIF allows detection of a significant increase of V_p (derived from the ETM) in PEGPH20 versus vehicle group (p < 0.05). Increase of V_p is consistent with a large increase of mean capillary lumen area estimated from immunostaining.

CONCLUSION:

Our results suggest that k_ep derived from SSM and V_p from ETM, both using group AIF, are optimal for the detection of microvascular changes induced by stroma-directed drug PEGPH20. These analyses provide insights in the choice of PK model and AIF for optimal DCE protocol design in mouse pancreatic cancer models.

News (Medical) associated with Pegvorhyaluronidase alfa

08 Sep 2023

·www.pmlive.com

ICR study finds way to determine efficacy of experimental breast cancer drugs

Researchers at The Institute of Cancer Research (ICR), London, have discovered a way to use a simple, non-invasive MRI scan to determine whether an experimental approach to enhance treatment for breast cancer is effective. New research from the study, funded by Cancer Research UK, could help doctors visualise tumours and speed up the development of targeted therapies for breast cancer. If successful, these drugs could enhance the effectiveness of other drugs administered in combination. Common features of breast cancer include excessive connective tissue, which consists of cells and fibres that provide a scaffold, known as the extracellular matrix (ECM), where tumours can grow. Hyaluronic acid, which works by absorbing water, is naturally present inside the tumour ECM and causes cancer tumours to swell, making it challenging for drugs to penetrate, reach and destroy cancer cells. Researchers are able to use experimental drugs that target and degrade a chemical called hyaluronic acid to dissolve some of the dense ECM and improve drug delivery to tumours. However, when using experimental drugs targeting the chemical in this way, it can be difficult for researchers to identify the exact time when the acid has been degraded, and therefore, it is a challenge to determine the best time to administer other drugs. The researchers performed multi-parametric MRI scans on mice with breast tumours to track the efforts of PEGPH20, an investigational drug targeting hyaluronic acid, to gain measurements that provide additional information about the tissue being analysed. Study leader, Simon Robinson, professor, magnetic resonance imaging of cancer, ICR, London, said: "Diffusion-weighted MRI can be performed on conventional clinical MRI scanners. Our new research shows that we can use such scans to check if [experimental] drugs like PEGPH20 are working, helping guide treatment in a more targeted and non-invasive way." For example, after using diffusion-weighted imaging to understand how water molecules moved within tissue, the researchers found that a measurement of water’s ability to move or spread, called the apparent diffusion coefficient (ADC), was reduced by up to 38% following administration of PEGPH20. The results suggest that PEGPH20 could make breast cancer tissue more accessible to chemotherapy drugs and could potentially improve treatment outcomes. Upon further necessary testing, the researchers hope to improve the development of targeted therapies for breast cancer and potentially other tumours.

05 Nov 2019

·www.bioportfolio.com

Theramex Buys Janssen’s Evorel Amid Ongoing HRT Shortages

Amid ongoing manufacturing issues with its own HRT patches, women’s health spin-out Theramex acquires global rights to Janssen’s Evorel patches... Related Stories Turkey’s Domestic Vaccine Production Drive Prompts New Partnerships Takeda Sheds Products, Employees To Stada In $660m Move Halozyme’s Spotlight Shifts To Enhanze Exclusively After PEGPH20 Fails In Phase III

Vaccine

20 Apr 2015

·www.biospace.com

Halozyme Therapeutics, Inc. Presents New Preclinical Data At AACR Annual Meeting, Announces Clinical Data Presentation At ASCO

SAN DIEGO, April 20, 2015 /PRNewswire/ -- Halozyme Therapeutics, Inc. (NASDAQ: HALO), a biotechnology company developing novel oncology and drug-delivery therapies, today shared highlights of new data it presented at the American Association for Cancer Research (AACR) annual meeting. Halozyme also announced plans to present interim results of its randomized Phase 2 study in pancreatic cancer, Study 202, next month at the annual meeting of the American Society of Clinical Oncology (ASCO). In an oral presentation at the AACR meeting titled "Hyaluronan (HA) Depletion Increases Tumor Accessibility of T cell and Therapeutic PD-L1 Monoclonal Antibody in HAhigh Tumors," findings in an animal model of non-small-cell lung cancer included: Tumors with high levels of HA a structural carbohydrate that accumulates in the areas surrounding cancer cells --form a natural HA-rich barrier that restricted T-cell access to tumor cells; Halozyme's investigational new drug, PEGPH20, depletes HA and increases T-cells access to tumor cells in an animal models; HA removal by PEGPH20 enhanced anti-PD-1 or anti-PD-L1 dependent tumor-cell killing in cell based assays; HA depletion by PEGPH20 increased the access of T cell and anti-human PD-L1antibody in HA-high xenograft tumors, suggesting that PEGPH20 may have the potential to enhance the efficacy of immune checkpoint inhibitors in human HA-high tumors This new preclinical data adds to the growing body of evidence, generated in multiple animal tumor models, demonstrating increased efficacy when a range of different cancer therapeutics are administered with PEGPH20. Halozyme also presented findings relevant to the development of a companion diagnostic test for PEGPH20 in a poster presentation titled, "Development and Analytical Validation of a Novel Assay for Tissue Detection of Hyaluronan in the Tumor Microenvironment to Select Patients for Molecularly Targeted Pancreatic Cancer Therapies." These findings include: Halozyme's companion diagnostic assay and proprietary HTI-601 binding probe were sensitive, specific and met the company's acceptability criteria for the detection and measurement of HA levels in archival samples from multiple different tumors types; and HTI-601 may be appropriate as a companion diagnostic approach for the selection of patients with high HA levels suitable for therapy using PEGPH20. The company announced on April 8 plans to proceed with a Phase 3 clinical study (Study 301) of PEGPH20 in patients with metastatic pancreatic cancer using a companion diagnostic to prospectively identify patients with high levels of HA. "The findings we presented at AACR highlight the progress we are making with PEGPH20 development, with the preclinical data providing further support for the initiation of the planned combination trial with a PD1 inhibitor in non-small-cell lung cancer," said Athena Countouriotis, senior vice president and chief medical officer. "The evidence of HTI-601 as a sensitive and specific assay for HA was one of the key steps in our plans to have the companion diagnostic ready for Phase 3 initiation in the first quarter of 2016." Two additional poster presentations at AACR will be presented today (April 20): Title: "PEGPH20 Enhances Chemotherapy in Patient-Derived and Traditional Cell-Derived Xenograft NSCLC Models" Abstract #: 2547, April 20, 2015, 1:00PM - 5:00PM EDT (Poster) Location: Section 27, Poster 29 Title: "Hyaluronan-Dependent Growth of Human Triple Negative Breast Cancer MDA-MB-468 in Mouse Xenograft Models" Abstract #: 2392, April 20, 2015, 1:00PM - 5:00PM EDT (Poster) Location: Section 19, Poster 25 ASCO Session Session titles posted today for next month's ASCO annual meeting included, "High Response Rate and PFS with PEGPH20 added to Nab-Paclitaxel/Gemcitabine in Stage IV Previously Untreated Pancreatic Cancer Patients with High-HA Tumors: Interim Results of a Randomized Phase 2 Study." During this session Dr. Sunil Hingorani, a principal investigator, will share interim results of Study 202, a phase 2 study of Halozyme's PEGPH20 combined with nab-paclitaxel (ABRAXANE®) and gemcitabine compared with nab-paclitaxel (ABRAXANE®) and gemcitabine alone in metastatic pancreatic cancer patients. About PEGPH20 PEGPH20 is an investigational PEGylated form of Halozyme's proprietary recombinant human hyaluronidase under clinical development for the systemic treatment of tumors that accumulate hyaluronan. FDA granted orphan drug designation to PEGPH20 for treatment of pancreatic cancer and fast track for PEGPH20 in combination with gemcitabine and nab-paclitaxel for the treatment of metastatic pancreatic cancer. Additionally, the European Commission, acting on the recommendation from the Committee for Orphan Medicinal Products of the European Medicines Agency, designated investigational drug PEGPH20 an orphan medicinal product for the treatment of pancreatic cancer. Clinical trials are currently ongoing for development of PEGPH20 in pancreatic ductal adenocarcinoma and in non-small cell lung cancer. More information may be found at: . About Halozyme Halozyme Therapeutics is a biotechnology company focused on developing and commercializing novel oncology therapies that target the tumor microenvironment. Halozyme's lead proprietary program, our investigational drug PEGPH20, applies a unique approach to targeting solid tumors, allowing increased access of co-administered cancer drug therapies to the tumor. PEGPH20 is currently in development for metastatic pancreatic cancer and non-small cell lung cancer and has potential across additional cancers in combination with different types of cancer therapies. In addition to its proprietary product portfolio, Halozyme has established value-driving partnerships with leading pharmaceutical companies including Roche, Pfizer, Janssen and Baxter for its drug delivery platform, ENHANZE, which enables biologics and small molecule compounds that are currently administered intravenously to be delivered subcutaneously. Halozyme is headquartered in San Diego. For more information on how we are innovating, visit . Safe Harbor Statement In addition to historical information, the statements set forth above include forward-looking statements (including, without limitation, statements concerning the possible activity, benefits and attributes of PEGPH20, the possible method of action of PEGPH20, its potential application to improve cancer therapies and statements concerning future actions relating to the development of PEGPH20) that involve risk and uncertainties that could cause actual results to differ materially from those in the forward-looking statements. The forward-looking statements are typically, but not always, identified through use of the words "believe," "enable," "may," "will," "could," "intends," "estimate," "anticipate," "plan," "predict," "probable," "potential," "possible," "should," "continue," and other words of similar meaning. Actual results could differ materially from the expectations contained in forward-looking statements as a result of several factors, including unexpected expenditures and costs, unexpected results or delays in development and regulatory review, regulatory approval requirements, unexpected adverse events and competitive conditions. These and other factors that may result in differences are discussed in greater detail in the Company's Annual Report on Form 10-K filed with the Securities and Exchange Commission on March 2, 2015. Contacts: Schond Greenway Halozyme Therapeutics 858-704-8352 ir@halozyme.com Jim Mazzola Halozyme Therapeutics 858-704-8122 ir@halozyme.com Logo - To view the original version on PR Newswire, visit: SOURCE Halozyme Therapeutics, Inc. Help employers find you! Check out all the jobs and post your resume.

CollaborateAntibodyOrphan DrugFinancial StatementSmall molecular drug

100 Deals associated with Pegvorhyaluronidase alfa

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R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Pancreatic Ductal Adenocarcinoma	Phase 3	US	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	AU	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	BE	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	BR	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	CA	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	HR	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	CZ	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	DK	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	EE	Halozyme Therapeutics, Inc.	14 Mar 2016
Pancreatic Ductal Adenocarcinoma	Phase 3	FR	Halozyme Therapeutics, Inc.	14 Mar 2016

Clinical Result

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


EASD2022	Not Applicable	Glomerular disease HA \| CD44 +	-	PEGPH20	cmnrvbnlih(kbzathveab) = iziobxwetj ooayssznrv (mjumqfwndl ) View more	Positive	22 Sep 2022
				Vehicle	cmnrvbnlih(kbzathveab) = hvpcauhwos ooayssznrv (mjumqfwndl ) View more
NCT03979066 (NEOiPANC, CTgov)	Phase 2	Pancreatic Ductal Adenocarcinoma	1	atezolizumab (Atezolizumab)	qlqiijnunh(ovaarausxr) = sajhacxmpx yrjllvshhw (fugjvnyafv, eiiopggwhf - lhovywxfee) View more	-	23 Dec 2020
				atezolizumab+PEGPH20 (Atezolizumab in Combination With PEGPH20)	qlqiijnunh(ovaarausxr) = xxawphtyqk yrjllvshhw (fugjvnyafv, xbmduhyzll - hylnhbrwof) View more
NCT02715804 (HALO 109-301, Pubmed \| J Urol) Manual	Phase 3	Pancreatic adenocarcinoma metastatic First line	492	Nab-Paclitaxel+Gemcitabine+Pegvorhyaluronidase Alfa	ebrmweyeke(enwhwkccmp) = bwvzppasri wnicwzlffv (auxwzypphg ) View more	Negative	20 Sep 2020
				Nab-Paclitaxel+Gemcitabine+Placebo	ebrmweyeke(enwhwkccmp) = budcirmxmx wnicwzlffv (auxwzypphg ) View more
NCT02715804 (HALO 109-301, CTgov)	Phase 3	Pancreatic Ductal Adenocarcinoma	492	nab-Paclitaxel+Gemcitabine (PAG: PEGPH20 + Nab-Paclitaxel + Gemcitabine)	ejjfomggey(owqmcjyevv) = tsmubxexqj pphxskhawm (dhzkgcmcdx, osfmpbgkhs - mtlbllxdbi) View more	-	14 Jul 2020
				Placebo+nab-Paclitaxel+Gemcitabine (AG: Placebo + Nab-Paclitaxel + Gemcitabine)	ejjfomggey(owqmcjyevv) = aumptpoeju pphxskhawm (dhzkgcmcdx, rzzqxuaasu - qatoadrtwi) View more
NCT03193190 \| NCT03281369 (ASCO2020) Manual	Phase 1/2	Pancreatic Ductal Adenocarcinoma \| Stomach Cancer Second line	133	atezolizumab+PEGPH20 (M-PDAC)	rppdmgcyji(nfhhvtneoa) = jwyxdhjnuw rdldcixqaf (lrhhctbqzi ) View more	Negative	25 May 2020
				mFOLFOX6 or gemcitabine + nab-paclitaxel (M-PDAC)	rppdmgcyji(nfhhvtneoa) = dzolbchagf rdldcixqaf (lrhhctbqzi ) View more
NCT01959139 (SWOG S1313 \| S1313, CTgov)	Phase 1/2	Pancreatic adenocarcinoma metastatic \| Secondary malignant neoplasm of pancreas	126	Leucovorin+Irinotecan+Oxaliplatin+5-fluorouracil (Phase II: mFOLFIRINOX)	jvjhzajars(lhivbcnubx) = giqhsvoxtd ztnpukvwgt (qldsipaqmi, jwwzfrvpvr - xsbcknzkqt) View more	-	12 Feb 2020
				Leucovorin+Irinotecan+Oxaliplatin+PEGPH20+5-fluorouracil (Phase II: mFOLFIRINOX + PEGPH20)	jvjhzajars(lhivbcnubx) = tflljeowrh ztnpukvwgt (qldsipaqmi, tzpxboxswv - qhvcpyjygz) View more
NCT03267940 (CTgov)	Phase 1	Intrahepatic Cholangiocarcinoma \| Gallbladder adenocarcinoma \| Unresectable Intrahepatic Cholangiocarcinoma	85	GEM+CIS+PEGPH20 (Run-in Portion: PEGCISGEM)	npijoremqv(vdgaefluxi) = igvuzudwxb zjrltpgvit (kidgiewbwp, dizafubndz - bzyzfchcza) View more	-	07 Feb 2020
				GEM+atezolizumab+CIS+PEGPH20 (Run-in Portion: PEGCISGEMATEZO)	npijoremqv(vdgaefluxi) = lczczqoyzq zjrltpgvit (kidgiewbwp, itxwexfakv - oooqfshkwe) View more
NCT02563548 (HALO 107-101, ESMO_ASIA2019)	Phase 1	Non-Small Cell Lung Cancer	21	PEGPH20	zasdzovcuc(gkzcwstjvo) = esphmwyadu nenxilsuzi (frtcoirxgs ) View more	-	23 Nov 2019
NCT01453153 (CTgov)	Phase 1/2	Pancreatic Cancer	28	PEGPH20 (PEGPH20 1.0 μg/kg)	tgohdtxvbx(tgcuswukpn) = ralumawcle lrdhhldtmt (vwzugtgxxp, cswhlscodu - qnrgscufml) View more	-	30 Nov 2018
				PEGPH20 (PEGPH20 1.6 μg/kg)	tgohdtxvbx(tgcuswukpn) = mbyfpmpbed lrdhhldtmt (vwzugtgxxp, jrfdlemmnp - ljjsvloydj) View more

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