Virulizin is an immunotherapy drug preparation that is thought to stimulate the patient's immune system, which in turn may slow the growth of tumors. It is presented in vials as a sterile preparation for IM injection. The purpose of the trial is to investigate if Virulizin in combination with gemcitabine provides better efficacy than gemcitabine alone (with placebo) against pancreatic cancer.Virulizin® efficacy will continue to be assessed if chemotherapy is changed to 5-Fluorouracil.

Start Date01 Jul 2002

Sponsor / Collaborator

Aptose Biosciences, Inc.

100 Clinical Results associated with Virulizin

100 Translational Medicine associated with Virulizin

100 Patents (Medical) associated with Virulizin

Literatures (Medical) associated with Virulizin

01 Aug 2021·Cancer MedicineQ3 · MEDICINE

Interleukin‐25: New perspective and state‐of‐the‐art in cancer prognosis and treatment approaches

Q3 · MEDICINE

ReviewOA

Author: Olegovna Zekiy, Angelina ; Gholizadeh Navashenaq, Jamshid ; Amir, Azwar ; Ebrahimi Nik, Maryam ; Gowhari Shabgah, Arezoo ; Ahmadi, Majid ; Gardanova, Zhanna R. ; Thangavelu, Lakshmi

AbstractCancer is a leading cause of death which imposes a substantial financial burden. Among the several mechanisms involved in cancer progression, imbalance of immune cell‐derived factors such as cytokines and chemokines plays a central role. IL‐25, as a member of the IL‐17 cytokine subfamily, exerts a paradoxical role in cancer, including tumor supportive and tumor suppressive. Hence, we have tried to clarify the role of IL‐25 and its receptor in tumor progression and cancer prognosis. It has been confirmed that IL‐25 exerts a tumor‐suppressive role through inducing infiltration of eosinophils and B cells into the tumor microenvironment and activating the apoptotic pathways. In contrast, the tumor‐supportive function has been implemented by activating inflammatory cascades, promoting cell cycle, and inducing type‐2 immune responses. Since IL‐25 has been dysregulated in tumor tissues and this dysregulation is involved in cancer development, its examination can be used as a tumor diagnostic and prognostic biomarker. Moreover, IL‐25‐based therapeutic approaches have shown promising results in cancer inhibition. In cancers in which IL‐25 has a tumor‐suppressive function, employing IL‐25‐enhancing approaches, such as Virulizin® and dihydrobenzofuran administration, has potentially inhibited tumor cell growth. On the other hand, in the case of IL‐25‐dependent tumor progression, using IL‐25 blocking methods, including anti‐IL‐25 antibodies, might be a complementary approach to the other anticancer agent. Collectively, it is hoped, IL‐25 might be a promising target in cancer treatment.

01 Dec 2008·Cancer Immunology, ImmunotherapyQ2 · MEDICINE

Virulizin® induces production of IL-17E to enhance antitumor activity by recruitment of eosinophils into tumors

Q2 · MEDICINE

Article

Author: Tania Benatar ; Sandy Der ; Xiaoping Gu ; Vivian Lee ; Jeff Lightfoot ; Hui Li ; Ningping Feng ; Ming Wang ; Jim A. Wright ; Ming Y. Cao ; Aiping H. Young ; Yoon Lee ; Hongnan Jin

Virulizin has demonstrated strong antitumor efficacy in a variety of human tumor xenograft models including melanoma, pancreatic cancer, breast cancer, ovarian cancer and prostate cancer. Our previous studies have demonstrated that macrophages, NK cells, and cytokines are important in the antitumor mechanism of Virulizin. Virulizin treatment of tumor bearing mice results in the expansion as well as increased activity of monocytes/macrophages and production of cytokines IL-12 and TNFalpha and activation of NK cells. In this study we show that the inflammatory cytokine IL-17E (IL-25) is induced by Virulizin treatment and is part of its antitumor mechanism. IL-17E is a proinflammatory cytokine, which induces a T(H)2 type immune response, associated with eosinophil expansion and infiltration into mucosal tissues. IL-17E was increased in sera of Virulizin-treated mice bearing human melanoma xenografts, compared to saline-treated controls, as shown by 2D gel electrophoresis and ELISA. Treatment of splenocytes in vitro with Virulizin resulted in increased IL-17E mRNA expression, which peaked between 24 and 32 h post-stimulation. Both in vitro and in vivo experiments demonstrated that B cells produced IL-17E in response to Virulizin treatment. Furthermore, Virulizin treatment in vivo resulted in increased blood eosinophilia and eosinophil infiltration into tumors. Finally, injection of recombinant IL-17E showed antitumor activity towards xenografted tumors, which correlated with increased eosinophilia in blood and tumors. Taken together, these results support another antitumor mechanism mediated by Virulizin, through induction of IL-17E by B cells, leading to recruitment of eosinophils into tumors, which may function in parallel with macrophages and NK cells in mediating tumor destruction.

01 Oct 2007·International ImmunopharmacologyQ2 · MEDICINE

Virulizin®, a novel immunotherapy agent, stimulates TNFα expression in monocytes/macrophages in vitro and in vivo

Q2 · MEDICINE

Article

Author: Xiaoping Gu ; Hongnan Jin ; Sandy Der ; Vivian Lee ; Ming Y. Cao ; Aiping H. Young ; Yoon Lee ; Ming Wang ; Pu Liu ; Jim A. Wright ; Ningping Feng ; Tania Benatar ; Jeff Lightfoot ; Hui Li

Virulizin, a novel biological response modifier, has demonstrated broad antitumor efficacy in a variety of human tumor xenograft models including melanoma, pancreatic cancer, breast cancer, ovarian cancer and prostate cancer. Previous studies have demonstrated a significant role of macrophages and NK cells in the antitumor mechanism of Virulizin. Increased activity and expansion of macrophages and NK cells has been observed in mice treated with Virulizin. In the present study, the effects of Virulizin on TNFalpha expression were investigated in vitro and in vivo. CD-1 nude mice were treated with Virulizin daily for 5 days. Quantitative RT-PCR demonstrated that the level of TNFalpha mRNA increased in peritoneal macrophages isolated from Virulizin-treated mice as compared to the control group. An increase in TNFalpha protein expression was also observed, as assessed by flow cytometric analysis. Increased levels of TNFalpha mRNA were seen in human tumor xenografts following treatment of tumor-bearing mice with Virulizin. In the presence of LPS, Virulizin also stimulated TNFalpha protein secretion and mRNA expression in human monocytic U937 cells and mouse macrophage RAW264.7 cells in vitro in a time- and dose-dependent manner. U937 cells treated with Virulizin showed a significantly enhanced cytotoxicity that was eliminated upon neutralization of TNFalpha. Virulizin also induced the phosphorylation of IkappaB, suggesting that induction of TNFalpha expression by Virulizin is mediated by activation of NFkappaB. The results indicate that Virulizin-induced TNFalpha expression contributes to modulation of immune responses and antitumor activities.

100 Deals associated with Virulizin

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KEGG	Wiki	ATC	Drug Bank
-	-	L03A	-

R&D Status

Approved

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Indication	Country/Location	Organization	Date
Colorectal Cancer	MX	-	01 Jan 1997
Kaposi Sarcoma	MX	-	01 Jan 1997
Melanoma	MX	-	01 Jan 1997
Pancreatic Cancer	MX	-	01 Jan 1997
Renal Cell Carcinoma	MX	-	01 Jan 1997
Stomach Cancer	MX	-	01 Jan 1997
Uterine Cervical Cancer	MX	-	01 Jan 1997

Developing

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Indication	Highest Phase	Country/Location	Organization	Date
Pancreatic Cancer	Preclinical	-	Aptose Biosciences, Inc.	01 Jul 2002

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ASCO2006	Phase 3	Pancreatic Cancer	434	Virulizin + Gemcitabine	(mjdohnlhml) = ffeshassnw esvokqvfum (ilsmnztahr )	-	20 Jun 2006
				Placebo + Gemcitabine	(mjdohnlhml) = mvldbofxwo esvokqvfum (ilsmnztahr )

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