The aim of the present study is to evaluate the prophylactic effect of Sitagliptin, Pioglitazone and Dapagliflozine on Isoprenaline induced myocardial infarction in type II diabetic rats.

Start Date30 Oct 2024

Sponsor / Collaborator

Al-Azhar University

NCT03351296

/ Active, not recruitingPhase 2IIT

Randomized Phase 2 Trial Of Two Chemotherapy Regimens Plus Or Minus Bevacizumab In Patients With Well Differentiated Pancreatic Neuroendocrine Tumors

Compare the effect of capecitabine (cape) + temozolomide (temo) and of 5FU + streptozotocin (strepto) given with a new schedule (LV5FU2 + strepto), two of the most used chemotherapy regimens in the treatment of well differentiated pancreatic neuroendocrine tumors alone or in combination with bevacizumab (beva) on progression-free survival (PFS) and compare the chemotherapy regimens alone or with beva (two by two design) on the same criteria.

Start Date26 Jun 2018

Sponsor / Collaborator

Institut Gustave Roussy EURL

[+1]

NCT02246127

/ CompletedPhase 3IIT

Randomized Open Label Study to Compare the Efficacy and Safety of Everolimus Followed by Chemotherapy With Streptozotocin- Fluorouracilo (STZ-5FU) Upon Progression or the Reverse Sequence, in Advanced Progressive Pancreatic NETs (pNETs)

The purpose of this study is to compare streptozotocin (STZ) vs everolimus as first line treatment for advanced pNET and to elucidate which sequence of STZ based chemotherapy and the mammalian Target of Rapamycin (mTOR) inhibitor, everolimus, gives better results in terms of second Progression Free Survival (PFS) in well differentiated and advanced pancreatic NETs.

Start Date27 Oct 2014

Sponsor / Collaborator

Novartis Pharmaceuticals Corp.

[+1]

100 Clinical Results associated with Streptozocin

100 Translational Medicine associated with Streptozocin

100 Patents (Medical) associated with Streptozocin

14,904

Literatures (Medical) associated with Streptozocin

01 Feb 2027·JOURNAL OF ETHNOPHARMACOLOGY

Dabushen decoction ameliorates diabetes-associated cognitive dysfunction in association with changes in PINK1/Parkin-related mitophagy

Article

Author: Wang, Xiaxia ; Feng, Kang ; Zhang, Fengrong ; Wei, Zhaohui ; Wan, Shengfang ; Guo, Aijia ; Li, Jinyu ; Feng, Tingting

ETHNOPHARMACOLOGICAL RELEVANCE:

Diabetes-associated cognitive dysfunction (DCD) is a common and serious central nervous system complication of type 2 diabetes mellitus (T2DM). Dabushen Decoction (DBSD), first recorded in Fuxingjue Zangfu Yongyao Fayao, is a traditional Chinese herbal formula used to tonify the kidney and replenish essence. DBSD has shown potential pharmacological value in the intervention of cognitive dysfunction; however, its neuroprotective mechanisms remain to be systematically elucidated.

AIM OF THE STUDY:

This study aimed to validate the mitigating effect of DBSD on DCD and to further investigate its mechanism.

MATERIALS AND METHODS:

Ultra-high-performance liquid chromatography coupled with Q Exactive Orbitrap high-resolution mass spectrometry (UHPLC-QE/MS) was used to analyze the chemical constituents of DBSD. Network pharmacology analysis was subsequently performed by integrating the SwissTargetPrediction, GeneCards, and OMIM databases. A T2DM rat model was established using a high-fat diet combined with streptozotocin (HFD/STZ), followed by oral administration of DBSD for 8 weeks. The overall pharmacological effects of DBSD were evaluated using the Morris water maze, Y-maze, and glucose and lipid metabolism-related indicators. Nissl staining and immunohistochemistry were used to assess pathological changes in hippocampal neurons, while transmission electron microscopy, ATP measurement, and JC-1 staining were used to evaluate hippocampal mitochondrial ultrastructure and function. ELISA was used to measure oxidative stress and inflammatory markers, and hippocampal proteomics was performed to analyze the potential biological processes involved. Finally, immunofluorescence colocalization and Western blotting were used to evaluate changes in PINK1/Parkin-mediated mitophagy markers.

RESULTS:

A total of 22 candidate circulating prototype compounds were putatively annotated by UHPLC-QE/MS. Network pharmacology identified 215 intersecting targets, and GO and KEGG enrichment analyses suggested that these targets were mainly involved in mitochondrial ATP synthesis, oxidative phosphorylation, and metabolic pathways. In vivo experiments showed that DBSD, particularly at the high dose, reduced FBG, FINS, OGTT-AUC, TC, TG, and LDL-C levels, increased HDL-C levels, and enhanced behavioral performance in the Morris water maze, as reflected by a greater number of platform crossings and longer time spent in the target quadrant. Histopathological results showed that DBSD increased the density of Nissl-positive neurons and the percentage of NeuN-positive cells in the hippocampal CA1 region and reduced Aβ immunoreactivity. In addition, DBSD ameliorated mitochondrial and synaptic ultrastructural damage, increased ATP levels, and improved mitochondrial membrane potential. DBSD reduced serum IL-1β, IL-18, and MDA levels as well as hippocampal NLRP3 protein expression, while increasing serum SOD and GSH levels. Proteomic analysis identified 82 shared differentially expressed proteins, which were mainly associated with mitochondrial energy metabolism, mitophagy, and synaptic function. Further validation showed that DBSD increased the percentage of LC3/TOMM20 colocalization-positive cells, significantly upregulated the expression of PINK1, Parkin, Beclin-1 and the LC3B-II/LC3B-I ratio, and downregulated p62, TOMM20, and COX IV protein expression in the hippocampus.

CONCLUSIONS:

DBSD improved cognitive function in rats with DCD, and its neuroprotective effects may be associated with changes in markers of PINK1/Parkin-mediated mitophagy and improved mitochondrial function.

01 Feb 2027·JOURNAL OF ETHNOPHARMACOLOGY

Gentianae Macrophyllae Radix inhibits renal fibrosis in type 2 diabetes via regulating aldose reductase

Article

Author: Zhang, Yazhou ; Ruan, Qingfeng ; Yang, Lu ; Xu, Zhanchi ; Han, Yue ; Mu, Kailan ; Wang, Qun ; Cheng, Xiaolan ; Wu, Tangqian ; Nong, Yanning

ETHNOPHARMACOLOGICAL RELEVANCE:

Gentianae Macrophyllae Radix (GMR), traditionally referred to as Qinjiao, consists of the desiccated roots derived from G. macrophylla Pall. Historically, this herb has been employed to alleviate edema, promote diuresis, quench thirst, and mitigate deficiency-related fever. Such clinical manifestations are commonly observed in patients suffering from diabetic kidney disease (DKD), a condition where renal fibrosis represents a critical pathological feature. Emerging evidence suggests that inhibiting aldose reductase (AR) could offer therapeutic benefits for DKD by ameliorating renal fibrosis. However, the scientific validation of GMR's efficacy in managing DKD remains lacking, and its potential influence on AR activity has not yet been investigated. Consequently, examining the capacity of GMR to modulate AR presents a promising avenue for DKD therapy.

AIM OF THE STUDY:

The present research conducted a thorough assessment of the anti-DKD properties of GMR with a specific focus on AR, intending to verify its therapeutic potency and elucidate the molecular mechanisms involved.

MATERIALS AND METHODS:

To investigate the therapeutic potential of GMR against DKD and AR, we developed both in vivo and in vitro experimental systems. The in vivo model utilized C57BL/6 mice subjected to a high-fat diet combined with streptozotocin administration, whereas the in vitro approach involved culturing glomerular mesangial cells under high-glucose conditions. Additionally, we identified the primary constituents of GMR capable of entering the bloodstream and evaluated their specific roles in modulating DKD and AR progression.

RESULTS:

This findings indicate that GMR treatment effectively attenuates renal fibrosis associated with DKD and suppresses AR activity by stimulating the nuclear factor erythroid-derived 2-related factor 2 (Nrf2) pathway, which subsequently lowers oxidative stress levels. Notably, when AR was over-expressed in cell cultures, it reversed the Nrf2 pathway activation induced by GMR, thereby diminishing the compound's ability to alleviate oxidative damage and reduce fibrotic changes. Further analysis revealed that swertiamarin is the principal bioactive component of GMR found in the circulation. This molecule directly binds to AR, leading to the regulation of oxidative stress responses and the amelioration of renal fibrosis.

CONCLUSION:

This research provides the initial evidence that GMR exerts a therapeutic effect on DKD by modulating AR activity, thereby mitigating oxidative stress. Swertiamarin, identified as the primary bioactive constituent in the bloodstream, functions as an inhibitor of AR.

01 Feb 2027·JOURNAL OF ETHNOPHARMACOLOGY

Integrative metabolomic and transcriptomic profiling uncovers the therapeutic mechanism of Qi Fu Yin in diabetic encephalopathy

Article

Author: Zhu, Yanrong ; Miao, Shan ; Shi, Xiaopeng ; Ma, Shanbo ; Li, Long ; Wang, Jin ; He, Yanru ; Lu, Chenxi ; Sun, Yang ; Guo, Xiaodi ; Zhang, Jing

ETHNOPHARMACOLOGICAL RELEVANCE:

Qi Fu Yin (QFY), a formulation derived from the "Jingyue Quanshu,"is reputed for its ability to tonify qi, nourish blood, replenish essence and marrow, and enhance cognitive functions. Clinical studies have demonstrated its significant efficacy in ameliorating cognitive impairments such as amnesia and dementia. Nevertheless, the therapeutic effects and mechanisms of QFY on cognitive dysfunction related to diabetic encephalopathy (DE) still require significant and in-depth research.

AIM OF THE STUDY:

This study aims to elucidate the efficacy and underlying mechanisms of QFY in the treatment of DE.

METHODS:

A DE model in C57BL/6J mice was established using a high-fat diet combined with intraperitoneal injection of streptozotocin. The improving effects of QFY on glucose and lipid metabolism disorders, cognitive dysfunction, and nerve damage in DE mice were systematically evaluated through behavioral experiments, biochemical indicator detection, and pathological staining of hippocampal tissues. The core regulatory pathways were identified using combined transcriptomic and metabolomic analyses. Additionally, RT-qPCR, Western blotting, immunofluorescence, and a high glucose-induced HT22 cell injury model were employed to verify the molecular mechanism of the AMPK/mTOR signaling pathway in regulating autophagy both in vivo and in vitro.

RESULTS:

QFY can significantly improve glucose and lipid metabolism disorders in DE mice, effectively reducing fasting blood glucose, glycated hemoglobin, and blood lipid levels. Meanwhile, it significantly increases SOD and GSH activities in hippocampal tissue, reduces MDA content, and alleviates oxidative stress damage. Behavioral and pathological test results show that QFY can significantly improve the spatial memory and cognitive function of DE mice, repair hippocampal neuronal structural damage, and inhibit neuronal apoptosis. Multi-omics integrated analysis confirmed that the AMPK/mTOR signaling pathway is the core pathway through which QFY intervenes in DE. In vivo and in vitro experiments further showed that QFY can activate the AMPK/mTOR pathway, upregulate the expression of the autophagy-related proteins Beclin1 and LC3, reduce p62 levels, and effectively inhibit high glucose-induced apoptosis by activating autophagy.

CONCLUSIONS:

QFY can enhance autophagy by activating the AMPK/mTOR signaling pathway, improve glucose and lipid metabolism disorders, reduce oxidative stress damage in DE mice, inhibit hippocampal neuron apoptosis, and thereby alleviate cognitive dysfunction associated with DE. This provides a new experimental basis for the treatment of diabetic encephalopathy with Traditional Chinese Medicine.

News (Medical) associated with Streptozocin

15 Feb 2024

·www.fiercebiotech.com

Sana's engineered pancreatic islet cells control blood sugar in monkey model of Type 1 diabetes

Sana Biotechnology is launching a clinical trial of its hypoimmune platform in humans through a Swedish university and expects to have data sometime in 2024. Sana Biotechnology’s genetically engineered pancreatic islet cells controlled glucose levels for six months in a diabetic primate without requiring insulin or immunosuppression, according to new preclinical data published online Feb. 13. The development is a step toward treating Type 1 diabetes without injectable insulin. In an article in the journal Cell Stem Cell, scientists from Sana reported that they had transplanted a primate version of the company’s islet cells—which are hypoimmune, meaning they have been genetically altered to avoid provoking an immune response—into a long-tailed macaque with Type 1 diabetes. “The results of this preclinical study are remarkable, and if they translate into the clinic, we have the potential to profoundly change the way that type 1 diabetes is addressed, potentially eliminating the need for insulin injections or immunosuppression,” Sana’s head of hypoimmune platform Sonja Schrepfer, M.D., Ph.D., said in a press release. The research is proof-of-concept for the company's hypoimmune platform, which will ultimately be paired with engineered islet cells grown from induced pluripotent stem cells, or iPSCs. Type 1 diabetes is an autoimmune condition that typically begins in childhood, though it can develop at any age. The disease is believed to arise from the immune system attacking the insulin-producing beta islet cells in the pancreas. To control their blood glucose levels, patients must take external insulin injections in some form—be it an insulin pump or shots multiple times a day—for the rest of their lives. Sana’s product for Type 1 diabetes, SC451, aims to replace a patient’s lost islet cells with genetically engineered ones that are derived from donors or grown from iPSCs. In the new study, they engineered islet cells taken from a macaque of a different species that had a markedly different genetic immune profile from the recipient—a way to show that the engineered therapy could work despite a high “immunological bar,” as Sana put it in the company's press release. Prior to the therapy, the recipient monkey was receiving two units of insulin per day to keep its blood sugar controlled. After the engineered islet cells were administered, the monkey was weaned off insulin at a rate of about half a unit every three days until it was completely discontinued. The monkey was followed for the next six months, over the course of which it didn’t receive any immunosuppressive therapy to prevent its immune system from rejecting the donor cells. The animal had “tightly controlled” blood sugar levels for the full six-month period without any insulin injections, and its levels of C-reactive protein—an inflammatory marker that has been shown to rise in organ transplant recipients at risk of graft rejection—remained stable as well. The monkey didn’t experience any behavioral or physical changes besides some mild weight gain, the researchers noted. Furthermore, analysis of T cells, natural killer cells, macrophages and antibodies showed no signs that the animal’s immune system was flaring up in response to the transplant. “These data demonstrate that our hypoimmune engineering completely circumvents allograft rejection, does not build immune memory, and thus achieves markedly better protection than systemic immunosuppression, and it is associated with no observed side effects,” the researchers wrote in the paper. “This successful NHP study provides proof of concept for an upcoming clinical trial using allogeneic, HIP-edited primary islets in patients with type 1 diabetes.” There are some limitations to the study. First, the researchers in this case induced destruction of the recipient monkey’s beta islet cells using a drug called streptozotocin. This is different from the autoimmune mechanisms that cause the disease in humans; however, previous positive results in mouse models of diabetes caused by autoimmunity suggest that it still works the same way, regardless of how the damage is caused. Second, there was no control animal in the study that received unedited islet cells due to evidence that they would be rejected, the researchers noted. Still, the evidence is enough to show that the concept is safe to test in humans. Sana is launching a clinical proof-of-concept study on the hypoimmune platform paired with donor-derived islet cells, UP421, through a Swedish university and expects to have data sometime this year, according to a Jan. 4 corporate presentation from the company.

Clinical StudyCell Therapy

21 Apr 2023

·www.biospace.com

Cancer And Diabetes Remain Among The Deadliest And Most Debilitating Diseases - Is Gene Therapy The Solution? One Company, Genprex, Inc. (NASDAQ: GNPX), Thinks So

AUSTIN, TX / ACCESSWIRE / April 19, 2023 / On their own, cancer or diabetes can be debilitating and deadly. The two are common diseases with tremendous impact on health worldwide. To make matters worse, epidemiologic evidence suggests that people with diabetes - especially Type 2 diabetes - are at significantly higher risk for many forms of cancer. The two pose a significant health problem and threat globally. In oncology, Genprex, Inc.(NASDAQ: GNPX) is initially focused on lung cancer. Annually, there are more than 2 million new cases of lung cancer worldwide with an average five-year survival rate of 18.6%. Over 537 million people worldwide suffer from diabetes with annual global mortality of about 6.7 million. Gene Therapy To The Rescue? Genprex Inc., a clinical-stage gene therapy company, is focused on developing for these patients with serious medical conditions and unmet need new and better treatment options that are life-changing. Founded in 2009 and headquartered in Austin, Texas, the company has been at the forefront of gene therapy research, focusing on harnessing the power of cutting-edge technologies to improve the lives of those affected by debilitating conditions. Driven by a deep commitment to scientific excellence and patient-centricity, Genprex reports that its mission is to revolutionize the treatment landscape by developing innovative gene therapies that have the potential to transform the lives of patients who have limited treatment options. Innovative Pipeline Genprex's oncology program utilizes the company's proprietary, non-viral ONCOPREX® Nanoparticle Delivery System, which it believes is the first systemic gene therapy delivery platform used for cancer in humans. ONCOPREX® encapsulates the gene-expressing plasmids using lipid nanoparticles, and the resultant product is administered intravenously, where it is then taken up by tumor cells in which tumor suppressor genes are missing or deficient. Genprex's value proposition lies in its robust and diversified pipeline of gene therapy candidates addressing large underserved patient populations, a strong intellectual property portfolio, and a seasoned management team with extensive experience in biopharmaceutical development and commercialization. The company's pipeline is anchored by its lead product candidate, REQORSA™ Immunogene Therapy (quaratusugene ozeplasmid), an innovative gene therapy that has been shown in pre-clinical testing to be potentially applicable to many types of cancer. Genprex is initially targeting non-small cell lung cancer (NSCLC) patients and small cell lung cancer (SCLC). REQORSA™ works by introducing a tumor suppressor gene (TUSC2) into cancer cells, inhibiting tumor growth and promoting cancer cell death. REQORSA™is being evaluated by Genprex as a treatment for NSCLC in two phase 1/2 clinical trials, with each trial receiving a Fast Track Designation ("FTD") from the U.S. Food and Drug Administration (FDA). One FTD is for use of REQORSA in combination with Merck & Co's Keytruda®, and the other is for use of REQORSA in combination with Astra Zeneca's Tagrisso REQORSA is also being evaluated for SCLC in combination with Genentech's Tecentriq with a trial expected to launch later this year. REQORSA has shown promise in preclinical and clinical studies, demonstrating its potential to improve patient outcomes in combination with other cancer treatments. Genprex sees the potential to use its proprietary gene therapy delivery platform to pursue a number of other cancer indications targeting the delivery of therapeutic genes to tumors as opposed to normal cells. The company's diabetes gene therapy approach comprises a novel infusion process that uses an endoscope and an adeno-associated virus (AAV) vector to deliver Pdx1 and MafA genes to the pancreas. In models of Type 1 diabetes, the genes express proteins that transform alpha cells in the pancreas into functional beta-like cells, which can produce insulin but are distinct enough from beta cells to evade the body's immune system. In Type 2 diabetes, where autoimmunity is not at play, it is believed that exhausted beta cells are rejuvenated and replenished. The company in February announced groundbreaking data from a non-human primate study evaluating its novel gene therapy to treat Type 1 diabetes. Results showed statistically significant decreases in insulin requirements, increases in c-peptide levels and improvements in glucose tolerance compared to baseline. The report was based on results from eight non-human primates (NHPs) with toxin-induced diabetes after streptozocin administration. They received a novel infusion process that used an AAV vector to deliver Pdx1 and MafA genes directly to the pancreas. Big Pharma's Bet On Gene Therapy Big Pharma is rapidly accelerating investment in emerging gene therapies with diabetes being of particular note. Major players, such as Eli Lilly and Company, Sanofi SA, and Novo Nordisk A/S, are advancing novel therapies that may supplant traditional insulin-based therapies. In April 2021, Jaguar Gene Therapy announced the closing of a $139 million Series B investment led by Eli Lilly and Company and Deerfield Management, to support the advancement of a novel gene therapy for type 1 diabetes. In March 2023, Sanofi announced the intention to acquire Provention Bio, and its TZIELD therapy that delays the onset of Type 1 diabetes, in a deal valued at approximately $2.9 billion. In April 2023, Novo Nordisk entered a collaboration with Aspect Biosystems to pursue novel therapeutics for Type 1 diabetes and obesity, in a deal valued at approximately $2.6 billion. Other big players like Amgen Inc., Gilead Sciences Inc., Biogen Inc., and bluebird bio Inc., have also made big bets in gene therapy. Intellectual Property Genprex's intellectual property portfolio - consisting of numerous issued patents and pending patent applications licensed from major academic research institutions - could provide the company with a strong competitive advantage in the gene therapy space. This IP protection covers key aspects of the company's proprietary technologies and product candidates, including methods of gene delivery, therapeutic compositions and manufacturing processes. Experienced Management Team The success of Genprex is driven by its experienced and dedicated management team, which brings decades of combined experience in biopharmaceutical development, commercialization, and business operations. This expertise could ensure that the company is well-positioned to navigate the complex landscape of gene therapy development and deliver on its mission to bring innovative treatments to large populations of patients in need. Genprex Strengthens Diabetes Gene Therapy Program On December 15 last year, the company announced it had entered into an exclusive license agreement with the University of Pittsburgh, granting Genprex a worldwide, exclusive license to certain patent applications and related technology and a worldwide, non-exclusive license to use certain related know-how, all related to modulating autoimmunity in Type 1 diabetes by using gene therapy. The preclinical technology transforms macrophages, enabling them to reduce autoimmune activity in Type 1 diabetes, and could be complementary to the company's existing diabetes technology. Genprex Signs Exclusive License To Additional Diabetes Technology The company also revealed on January 5 that it has entered into another exclusive license agreement with the university, granting Genprex a worldwide, exclusive license to a patent application and related technology and a worldwide, non-exclusive license to use certain related know-how, all related to gene therapy for Type 2 diabetes using the genes of the Pdx1 and MafA transcription factors. The preclinical technology, GPX-003, is believed to work by rejuvenating diminished beta cells to increase insulin expression by introducing transcription factors controlled by an insulin promoter. Featured photo sourced from Shutterstock CONTACT: Genprex investors@genprex.com SOURCE: Genprex View source version on accesswire.com:

License out/inGene TherapyClinical StudyAcquisitionFast Track

13 Mar 2023

·www.biospace.com

CRISPR/ViaCyte and Genprex Vie for First Diabetes Gene Therapy

A female Researcher works with vials of blood/courtesy of Getty Images Genome editing has been a hot-button topic in recent years. With the rise of CRISPR technology in the news, this is not surprising for either scientists or investors. In February 2022, CRISPR Therapeutics and ViaCyte made history, carrying out the first-in-human transplant of gene-edited, stem cell-derived pancreatic cells to treat Type 1 diabetes (T1D). With results of an animal study published in February 2023, Genprex aims to add credibility to another genome editing approach in the hunt for a functional cure to T1D. Based in Austin, Texas, Genprex focuses on developing life-changing therapies for cancer and diabetes. The company’s pipeline includes three different products under investigation: Reqorsa, GPX-002 and GPX-003. While Reqorsa is seeking indications in cancer in Phase I trials, GPX-002 and GPX-003 are undergoing preclinical trials for diabetes, with GPX-002 targeting T1D and GPX-003 targeting type 2 diabetes (T2D). While traditional gene therapies include replacement gene therapy, gene editing and CAR-T for diabetes, Genprex aims to use Adeno-Associated Virus (AAV) pancreatic intraductal infusions to deliver Pdx1 and MafA genes to the pancreas. Non-Human Primate Study One month after eight non-human primates (NHPs) were injected with streptozocin to induce diabetes, surgical procedures were performed to provide infusions to the subjects. Results showed the NHPs had decreased insulin requirements, increased C-peptide levels, improved glucose tolerance compared to baseline and more insulin-positive cells compared to non-treated diabetic controls based on immunohistochemistry. The researchers assessed blood glucose and insulin requirements. During the untreated diabetes induction period, total daily exogenous insulin levels were between 8 and 10 units and average daily blood glucose levels were between 50 and 100 mg/dL. After Genprex’s investigational AAV-CMV-Pdx1-mafA construct was injected during the surgical procedure, average daily blood glucose levels spiked to 200 mg/dL initially, but total daily exogenous insulin levels decreased to below 4 units. Average daily blood glucose levels decreased to around 100 mg/dL 56 days after the operation. Average glucose stimulated insulin secretion remained higher following the operation compared to prior, and eight weeks after the operation, glucose suppression capabilities improved. At the 3-month mark, NHP2 recent glucose tolerance test results showed there was virtually no difference between treated diabetic NHPs at the 3-month mark versus healthy NHPs. While this achievement may seem to be revolutionary, there are unknowns that need to be assessed. Genprex stated the gene therapy could be administered without an operation using routine endoscopic retrograde cholangiopancreatography in humans, but this is a different type of procedure from the one used on NHPs. In addition, the allure of a quick cure to diabetes may require some cultural acceptance for patients used to lifelong interventions such as oral and injectable treatments. Finally, Genprex’s human trials have yet to commence, so FDA approval for this type of treatment may not hit the market until the latter half of the 2020s at the earliest. CRISPR and ViaCyte in Phase I CRISPR and ViaCyte are slightly further ahead with their diabetes genome editing treatment, VCTX210. This was a key attraction for Vertex, which acquired ViaCyte in July 2022. While previous products from ViaCyte such as PEC-Direct require long-term immunosuppression with drugs, VCTX210 is designed to be a more permanent solution without the need for immunosuppressants. As of February 2023, the companies had completed dosing in Phase I subjects. While this is technically one step ahead of Genprex, the Phase I trial is primarily looking at safety as opposed to efficacy data. There are also some differences between VCTX210 and Genprex’s products. VCTX210 is an allogeneic, gene-edited, stem cell-derived therapy designed as a best-in-class treatment for T1D and insulin-dependent T2D, while Genprex uses viral delivery. Regardless of what the future holds for Genprex versus CRISPR/Viacyte, these gene therapy agents hold much promise in the search for a single solution to diabetes. With potential answers for a patient pool that numbers in the hundreds of millions worldwide, keep an eye out for these frontrunners in the next few years.

Gene TherapyPhase 1Clinical Result

100 Deals associated with Streptozocin

External Link

KEGG	Wiki	ATC	Drug Bank
D05932	Streptozocin	L01AD04	DB00428

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Gastro-Enteropancreatic Neuroendocrine Tumor	Japan	Nobelpharma Co., Ltd.	26 Sep 2014
Pancreatic Cancer	United States	Teva Pharmaceuticals USA, Inc.	07 May 1982

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESMO_MAP2026	Not Applicable	Advanced Neuroendocrine Neoplasm Ki-67	26	Streptozotocin-based chemotherapy (Ki-67 ≤50%)	tuqkfpjfss(xuptoeoinw) = zhihmwmizm nthypdruce (bjyzldzcpz )	Positive	10 Sep 2026
				Streptozotocin-based chemotherapy (Ki-67 >50%)	tuqkfpjfss(xuptoeoinw) = ajwmuyghbr nthypdruce (bjyzldzcpz )
NCT02246127 (SEQTOR \| GETNE-1206, CTgov)	Phase 3	Advanced Pancreatic Neuroendocrine Tumor	141	STREPTOZOCIN+Drug: Everolimus+FLUOROURACIL (Sequence A, Drug: Everolimus First)	huuryxlucf = vjhrriomvr yttvzreagv (wduzpjftsv, ncxpdgkqrd - cywoterank) View more	-	11 May 2025
				STREPTOZOCIN+Drug: Everolimus+FLUOROURACIL (Sequence B, Drug: STZ - 5FU First)	huuryxlucf = phdyykqbhq yttvzreagv (wduzpjftsv, jjiulsznfl - psugemounq) View more
NCT02246127 (GETNE-1206, ESMO2024)	Phase 3	Advanced Pancreatic Neuroendocrine Tumor	141	Everolimus	qywpnkonhu(wadwnzyaec) = ybvkvvscsb jmsnjeyinq (oyciismwes ) View more	Positive	16 Sep 2024
				STZ/5-FU	qywpnkonhu(wadwnzyaec) = nvgnrnwozh jmsnjeyinq (oyciismwes ) View more
NCT00094497 (FIRM-ACT, ENDO2024)	Phase 3	Adrenocortical Carcinoma Second line	-	Streptozotocin and Mitotane (SM)	vpblyetcij(qszdtkpoyr) = adequately replaced adrenal and thyroid insufficiencies uagesykxnj (ugzvfikzau ) View more	Positive	01 Jun 2024
NCT02246127 \| EUCTR2013-000726-66-DE (GETNE 1206, ESMO2022) Manual	Phase 3	Advanced Pancreatic Neuroendocrine Tumor	141	STZ-5FU+Everolimus 10 mg/day (arm A)	nedzihndig(zebmknbwhs) = kcuihnilpe wzqkzqvotr (kkigoirxiu ) View more	Positive	12 Sep 2022
				STZ-5FU+Everolimus 10 mg/day (arm B)	nedzihndig(zebmknbwhs) = fzltjvhbxq wzqkzqvotr (kkigoirxiu ) View more
NCT00094497 (FIRM-ACT, CTgov)	Phase 3	Adrenocortical Carcinoma	304	Etoposide+Doxorubicin+Cisplatin+Mitotane (EDP-M)	rhvcruiiza = pjrcanugsz ookbzxhlei (gkiaufydlj, gtbyltizxi - zatteseotc) View more	-	21 Sep 2016
				Streptozotocin+Mitotane (Sz-M)	rhvcruiiza = pqxndidwsz ookbzxhlei (gkiaufydlj, stgjvhbzzl - wzhohvuvpj) View more
ASCO2015	Not Applicable	Advanced Neuroendocrine Neoplasm	22	Streptozocin	jykncvdkqq(yuinjthvjr) = ycsgfkootu pwwvwvnuns (ibvmsfodtz ) View more	-	20 May 2015
ASCO_GI2014	Not Applicable	Neuroendocrine tumor of pancreas	95	STZ+5-FU chemotherapy	alncqpptza(ekclxsbvis) = junbhgvcsf xnopcinwez (ocxdalvmnv )	Positive	20 Jan 2014
ASCO2012	Phase 1	Liver metastases	19	HA FUDR	qrhjsiwqnv(jhyjrfinox) = mthoxqaqdt gaamvlzjjl (tvexejjglr ) View more	-	20 May 2012
BETTER study (ASCO2012)	Phase 2	Well Differentiated Pancreatic Endocrine Tumor	34	Bevacizumab + 5-FU/streptozotocin	zhvaikispg(ouctslzkyl) = ekgejkhlpy ykeeneshso (vwtkesznur ) View more	Positive	20 May 2012

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