Introgen Therapeutics is a biopharmaceutical corporation dedicated to discovering, developing, and commercializing targeted molecular therapies for cancer and other diseases. The company specializes in the creation of molecular therapeutics, immunotherapies, vaccines, and nano-particle tumor suppressor therapies to treat various types of cancer using tumor suppressors, cytokines, and genes. With integrated research, development, manufacturing, clinical, and regulatory departments, Introgen operates several manufacturing facilities, including a commercial-scale cGMP manufacturing facility. Founded in June 1993, the company is headquartered in Austin, TX.

Drugs associated with Introgen Therapeutics, Inc.

INGN-101

Target-

Mechanism-

Active Org.-

Originator Org.

Introgen Therapeutics, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date-

INGN-241

Target

IL-24

Mechanism

IL-24 stimulants

Active Org.-

Originator Org.

The Trustees of Columbia University in The City of New York

Active Indication-

Inactive Indication

Breast Cancer [+4]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date-

Contusugene ladenovec(Introgen Therapeutics, Inc.)

Target

p53

Mechanism

p53 modulators

Active Org.-

Originator Org.

Introgen Therapeutics, Inc.

Active Indication-

Inactive Indication

Bladder Cancer [+11]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date-

Clinical Trials associated with Introgen Therapeutics, Inc.

NCT00041613 / Unknown statusPhase 3

Study to Compare the Overall Survival of Patients Receiving INGN 201 (Study Drug) With Patients Receiving Methotrexate

There is a need for more treatment options for patients with recurrent squamous cell cancer of the head and neck (SCCHN). These tumors usually have a variety of genetic defects that include disruption of the p53 pathway, a pathway that would ordinarily work to prevent the development of tumors. In this study the transfer of the p53 gene to tumor cells using a modified adenovirus (INGN 201) will be compared to methotrexate in patients who have failed surgery, radiotherapy and chemotherapy with platinum or taxanes.

Start Date-

Sponsor / Collaborator

Introgen Therapeutics, Inc.

NCT00116363 / Unknown statusPhase 2

Phase II Study Examining the Biological Efficacy of Intratumoral INGN 241 (Ad-mda7) Administration in Patients With In Transit Melanoma

This is a research study to look at the ways in which a treatment called INGN241 can kill melanoma cells or help the patient's immune system kill melanoma cells.

Start Date01 Mar 2005

Sponsor / Collaborator

Introgen Therapeutics, Inc.

[+1]

NCT00044993 / CompletedPhase 2

Phase II, Single Arm, Single Institution Clinical Trial of Docetaxel and Doxorubicin in Combination With Local Administration of INGN 201 (Ad5CMV-p53) in Locally Advanced Breast Cancer (LABC)

RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Inserting the p53 gene into the tumor may increase the effectiveness of a chemotherapy drug by making tumor cells more sensitive to the drug. Combining chemotherapy with gene therapy may kill more tumor cells.
PURPOSE: Phase II trial to study the effectiveness of combining chemotherapy with gene therapy in treating patients who have stage III or stage IV breast cancer.

Start Date01 Feb 2002

Sponsor / Collaborator

Introgen Therapeutics, Inc.

100 Clinical Results associated with Introgen Therapeutics, Inc.

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

Literatures (Medical) associated with Introgen Therapeutics, Inc.

01 Oct 2009·Journal of Biological ChemistryQ2 · BIOLOGY

Structural Mapping of Post-translational Modifications in Human Interleukin-24

Q2 · BIOLOGY

Article

Author: Sunil Chada ; Molly Craxton ; Kerry L. Fuson ; R. Bryan Sutton ; Mingzhong Zheng ; Abujiang Pataer ; Rajagopal Ramesh

Human interleukin-24 (IL-24) is unique among the IL-10 superfamily as there is considerable evidence that it possesses multiple anti-cancer properties, including direct tumor cell cytotoxicity, helper T cell (TH1) immune stimulation, and anti-angiogenic activities. The primary sequence of human IL-24 differs from homologous cytokines, because it possesses three consensus N-linked glycosylation sites and the potential for a single disulfide bond. To address the significance of these modifications in human IL-24, we analyzed the relationship between post-translational modifications and the cytokine activity of the human IL-24 protein. In contrast to related interleukins, we identified a relationship between net glycosylation, protein solubility, and cytokine activity. In addition, abrogation of the two cysteine residues by mutagenesis dramatically altered the ability of IL-24 to secrete from host cells and resulted in the concomitant loss of IL-24 activity. We conclude that, unlike other IL-10 family members, human IL-24 must be glycosylated to maintain solubility and bioavailability. Further, a single, unique disulfide bond is required for secretion and activity. These structure-function relationships show that, although IL-24 is a member of the IL-19 subfamily of IL-10-like cytokines by sequence similarity, its surface properties and its distinctive disulfide arrangement make it unique. These observations could explain the novel biological activities measured of this cytokine. Understanding the structural basis of IL-24 activity will be important in the interpretation of the function of this cytokine and in the development of scale-up strategies for biophysical and clinical applications.

01 Dec 2008·International ImmunopharmacologyQ2 · MEDICINE

Closing the manufacturing process of dendritic cell vaccines transduced with adenovirus vectors

Q2 · MEDICINE

Article

Author: Dumrul Gulen ; Elizabeth Reed ; Samuel Pirruccello ; Sarah Maas ; Orhan Turken ; Matt Northam ; Fuminori Abe ; Joe Senesac ; James E. Talmadge ; James Wisecarver ; Ugur Coskun ; Phyllis Warkentin ; Kenneth Cowan

Anticancer immunotherapy using dendritic cell (DC) based vaccines provides an adjuvant therapeutic strategy that is not cross reactive with conventional therapeutics. However, manufacturing of DC vaccines requires stringent adherence to Good Manufacturing Practice (GMP) methods and rigorous standardization. Optimally this includes a closed system for monocyte isolation, in combination with closed culture and washing systems and an effective vector transduction strategy. In this study, we used the Gambro Elutra to enrich monocytes from non-mobilized leukapheresis products collected from healthy donors. This approach enriched monocytes from an average frequency of 13.6+3.2% (mean+SEM), to an average frequency of 79.5+4.3% following enrichment with a yield of 79 to 100%. The monocytes were then cultured in a closed system using gas permeable Vuelife fluoroethylene propylene (FEP) bags and X-vivo-15 media containing 10 ng/ml granulocyte-macrophage colony-stimulation factor (GM-CSF) and 5 ng/ml Interleukin (IL) 4. The cultures were re-fed on days two and four, with a 25% media volume and cytokines. Following culture for seven days, the cells were harvested using a Cobe-2991 and concentrated using a bench centrifuge retrofitted with blocks to allow centrifugation of 72 ml bags and supernatant removed using a plasma extractor. This approach reduced the media volume to an average of 17.4 ml and an average DC concentration of 6.3+1.0x10(7) cells/ml, a viability of 93.8+2.2%, a purity of 88.9+3.3% and a total yield of 8.5+1.4x10(8) DCs. Based on the identification of DR+ cells as DCs we had an average yield of 46+8% using a calculation based on the number of monocytes in the apheresis product and the resulting DCs differentiated from monocytes. The use of DCs as a vaccine, required transduction with an adenovirus (Adv) vector with the tumor suppressor, p53 transgene (Adv5CMV-p53) as the antigen at a DC concentration of 9x10(6) DCs/ml at an Ad5CMV-p53: DC ratio of 20,000:1, and a 2 or 3 hour co-culture, followed by a 1:10 dilution with media and an additional 16-22 hour incubation. Following incubation, the DCs were washed twice and the supernatants removed using a plasma extractor. The average viability after infection with Ad5CMV-p53 was 87.9+/-2.6% with an average of 20.3+5.4% of the DCs expressing p53. The calculated yield of DCs following Ad5CMV-p53 transduction, based on the number of monocytes in the apheresis products, averaged 12.4+3.8%. We conclude that it is possible to efficiently manufacture Adv transduced DCs using a functionally closed system.

01 Dec 2008·Molecular Cancer TherapeuticsQ2 · MEDICINE

Interleukin-24 overcomes temozolomide resistance and enhances cell death by down-regulation of O6-methylguanine-DNA methyltransferase in human melanoma cells

Q2 · MEDICINE

Article

Author: Ramesh, Rajagopal ; Bocangel, Dora ; Poindexter, Nancy ; Ekmekcioglu, Suhendan ; Grimm, Elizabeth A. ; Chada, Sunil ; Zheng, Mingzhong

AbstractMelanoma is the most malignant of skin cancers, highly resistant to chemotherapy and radiotherapy. Temozolomide, a promising new derivative of dacarbazine, is currently being tested for treatment of metastatic melanoma. Resistance to alkylating agents such as temozolomide correlates with increased expression of DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT). Interleukin-24 (IL-24; mda-7) is a tumor suppressor cytokine that selectively inhibits tumor cell growth by inducing apoptosis and cell cycle arrest in melanoma cell lines and solid tumors. This tumor-selective activity has been observed in multiple preclinical animal models and in clinical trials. In this study, we analyzed the ability of Ad-IL-24 and its protein product, IL-24, to overcome temozolomide resistance in human melanoma cells. We have shown that Ad-IL-24 via exogenous IL-24 protein induces combinatorial synergy of temozolomide-induced cell killing in temozolomide-resistant melanoma cells by inhibition of MGMT. Neutralizing antibodies against IL-24 or its receptors significantly blocked the apoptotic activity of IL-24 + MGMT treatment. We show that accumulation of functional p53 is essential for IL-24-induced down-regulation of MGMT. Using either MGMT small interfering RNA, p53 small interfering RNA, or a p53 dominant-negative mutant to block MGMT protein expression resulted in increased sensitization to temozolomide. However, MGMT blockade in combination with IL-24 + temozolomide resulted in loss of combinatorial synergy, indicating that MGMT expression is required for the reversal of temozolomide resistance in melanoma cells. This study shows that IL-24 can play a significant role in overcoming temozolomide resistance and that the clinical efficacy of temozolomide may be improved by using a biochemotherapy combination with IL-24. [Mol Cancer Ther 2008;7(12):3842–51]

100 Deals associated with Introgen Therapeutics, Inc.

100 Translational Medicine associated with Introgen Therapeutics, Inc.

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Pipeline

Pipeline Snapshot as of 28 Sep 2024

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

Other

Current Projects

Drug(Targets)	Indications	Global Highest Phase

INGN-101	Neoplasms More	Discontinued
Contusugene ladenovec(Introgen Therapeutics, Inc.) ( p53 )	Esophageal Carcinoma More	Discontinued
INGN-241 ( IL-24 )	Pancreatic Cancer More	Discontinued
INGN-234 ( p53 )	Vitiligo More	Discontinued
Tumour Suppressing Gene Therapies(Introgen) ( p53 )	Solid tumor More	Discontinued

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