Phase 2 Study of 9-ING-41, a Glycogen Synthase Kinase 3 Beta (GSK 3β) Inhibitor, Plus Carboplatin in Patients With Advanced, Metastatic Salivary Gland Carcinoma

9-ING-41 is a small molecule potent selective GSK-3β inhibitor with antitumor activity. This study investigates 9-ING-41 in combination with carboplatin chemotherapy in patients with incurable, recurrent or metastatic salivary gland carcinomas (SGC). Patients with advanced SGC (including all histologic subtypes and adenoid cystic carcinoma [ACC]) will receive 9-ING-41 intravenously (IV) along with carboplatin IV at standard dosing together on Day 1, and 9-ING-41 alone on Day 4 of a 21-day cycle. Participants will be enrolled to two histologic cohorts: Cohort 1 will be comprised of those with ACC, and Cohort 2 will include patients with non-ACC SGC (or all other salivary gland cancer histologies). Treatment will continue until progression of disease, death, or discontinuation of therapy for any reason.

Start Date18 Dec 2030

Sponsor / Collaborator

Actuate Therapeutics, Inc.Startup

NCT05077800

/ RecruitingPhase 2IIT

A Phase II Study of FOLFIRINOX Combined With the Glycogen Synthase Kinase-3 Beta (GSK-3 β) Inhibitor 9-ING-41 and the Transforming Growth Factor-β (TGF-β) Inhibitor Losartan in Patients With Untreated Metastatic Pancreatic Cancer

The purpose of this study is to find out if an experimental drug will prevent metastatic pancreatic adenocarcinoma from becoming resistant to standard treatment for the disease.
The names of the study drugs involved in this study are:
* 9-ING-41
* Losartan
* Ferumoxytol
* FOLFIRINOX (made up of 4 different drugs):
* 5-Fluorouracil (5-FU)
* Oxaliplatin
* Irinotecan
* Leucovorin

Start Date21 Mar 2022

Sponsor / Collaborator

Actuate Therapeutics, Inc.Startup

[+1]

NCT05116800

/ WithdrawnPhase 2IIT

A Phase 2 Study of 9-ING-41, a Glycogen Synthase Kinase-3 Beta (GSK-3β) Inhibitor, Combined With Chemotherapy in Advanced Soft Tissue and Bone Sarcomas

This is an open label, two-stratum, phase 2 clinical trial evaluating the efficacy of 9-ING-41 in combination with gemcitabine/docetaxel in patients ≥10 years of age with advanced sarcoma. 9-ING-41 in combination with gemcitabine and docetaxel will lead to sustained disease control and/or increase the rates of objective response in patients with unresectable or metastatic soft tissue and bone sarcomas.

Start Date01 Mar 2022

Sponsor / Collaborator

Brown University

[+1]

100 Clinical Results associated with Elraglusib

100 Translational Medicine associated with Elraglusib

100 Patents (Medical) associated with Elraglusib

Literatures (Medical) associated with Elraglusib

01 Dec 2024·EUROPEAN JOURNAL OF HAEMATOLOGY

A New Strategy for Adult T‐Cell Leukemia Treatment Targeting Glycogen Synthase Kinase‐3β

Article

Author: Ishikawa, Chie ; Mori, Naoki

ABSTRACT:

Objectives:

The role of glycogen synthase kinase (GSK)‐3β in adult T‐cell leukemia (ATL) caused by human T‐cell leukemia virus type 1 (HTLV‐1) is paradoxical and enigmatic. Here, we investigated the role of GSK‐3β and its potential as a therapeutic target for ATL.

Methods:

Cell proliferation/survival, cell cycle, apoptosis, and reactive oxygen species (ROS) generation were examined using the WST‐8 assay, flow cytometry, and Hoechst 33342 staining, respectively. Expression of GSK‐3β and cell cycle/death‐related proteins, and survival signals was analyzed using RT‐PCR, immunofluorescence staining, and immunoblotting.

Results:

HTLV‐1‐infected T‐cell lines showed nuclear accumulation of GSK‐3β. GSK‐3β knockdown and its inhibition with 9‐ING‐41 and LY2090314 suppressed cell proliferation/survival. 9‐ING‐41 induced G2/M arrest by enhancing the expression of γH2AX, p53, p21, and p27, and suppressing the expression of CDK1, cyclin A/B, and c‐Myc. It induced caspase‐mediated apoptosis by decreasing the expression of Bcl‐xL, Mcl‐1, XIAP, c‐IAP1/2, and survivin, and increasing the expression of Bak and Bax. 9‐ING‐41 also induced ferroptosis and necroptosis, promoted JNK phosphorylation, and suppressed IKKγ and JunB expression. It inhibited the phosphorylation of IκBα, Akt, and STAT3/5, induced ROS production, and reduced glycolysis‐derived lactate levels.

Conclusion:

GSK‐3β functions as an oncogene in ATL and could be a potential therapeutic target.

01 Nov 2024·Cancer research communications

Elraglusib Induces Cytotoxicity via Direct Microtubule Destabilization Independently of GSK3 Inhibition

Article

Author: Sutherland, Calum ; Tanaka, Tomoyuki U. ; Saurin, Adrian T. ; Li, Shuyu ; Tauro, Sudhir ; Coats, Josh T.

Abstract:

Elraglusib (9-ING-41) is an ATP-competitive inhibitor of glycogen synthase kinase-3 (GSK3) with preclinical studies demonstrating broad activity against many tumor types. Promising early-phase clinical trial data led to FDA orphan drug status, and a randomized phase II study in combination with cytotoxic chemotherapy in pancreatic cancer has recently completed its recruitment. Similarly, single-agent responses in adult T-cell leukemia/lymphoma and melanoma and combination treatment data in several other tumor types have been encouraging. The elraglusib mechanism of action is unknown, but it is unlikely to act through GSK3 inhibition because cytotoxicity is observed below the IC50 for GSK3, and other small molecule GSK3 inhibitors do not produce cytotoxic effects, at least in lymphoma cells. We show here that elraglusib perturbs chromosomal alignment to cause a mitotic arrest in multiple tumor lines. This arrest is caused by direct microtubule (MT) depolymerization, which prevents the attachment of kinetochores to MTs. At clinically relevant doses, these mitotically arrested cells eventually undergo mitotic slippage, leading to gross chromosome missegregation, DNA damage, and apoptosis. These effects explain the cytotoxicity of elraglusib because temporarily pausing cell-cycle progression with the CDK4/6 inhibitor palbociclib abolishes any drug-induced genotoxicity and apoptosis. In summary, elraglusib acts as a direct MT destabilizer both in vitro and across multiple cancer types, resulting in mitotic arrest, DNA damage, and apoptosis. These effects likely account for its broad pan-cancer activity, which does not rely upon GSK3 inhibition as they are not replicated by other GSK3 inhibitors.

Significance::

Elraglusib was designed as a GSK3 inhibitor and is currently in clinical trials for several cancers. We show conclusively that the target of elraglusib that leads to cytotoxicity is MTs and not GSK3. This has significant implications for ongoing clinical trials of the compound and will help in understanding off-target side effects, inform future clinical trial design, and facilitate the development of biomarkers to predict response.

01 Jun 2024·JHEP Reports

Glycogen synthase kinase 3 activity enhances liver inflammation in MASH

Article

Author: Islam, Shahidul ; Kim, Iljung ; Pavelko, Kevin D ; Mazar, Andrew P ; Li, Hu ; Warasnhe, Khaled ; Bamidele, Adebowale O ; Noh, Yung-Kyun ; Ibrahim, Samar H ; Kim Lee, Hyun Se ; Holmes, Heather ; Furuta, Kunimaro ; Valenzuela-Pérez, Lucía ; Guo, Qianqian ; Romero, Michael F ; Khoury, Mireille ; Correia, Cristina ; Sussman, Caroline R ; Meroueh, Chady ; Hirsova, Petra

Background & Aims:

Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by excessive circulating toxic lipids, hepatic steatosis, and liver inflammation. Monocyte adhesion to liver sinusoidal endothelial cells (LSECs) and transendothelial migration (TEM) are crucial in the inflammatory process. Under lipotoxic stress, LSECs develop a proinflammatory phenotype known as endotheliopathy. However, mediators of endotheliopathy remain unclear.

Methods:

Primary mouse LSECs isolated from C57BL/6J mice fed chow or MASH-inducing diets rich in fat, fructose, and cholesterol (FFC) were subjected to multi-omics profiling. Mice with established MASH resulting from a choline-deficient high-fat diet (CDHFD) or FFC diet were also treated with two structurally distinct GSK3 inhibitors (LY2090314 and elraglusib [9-ING-41]).

Results:

Integrated pathway analysis of the mouse LSEC proteome and transcriptome indicated that leukocyte TEM and focal adhesion were the major pathways altered in MASH. Kinome profiling of the LSEC phosphoproteome identified glycogen synthase kinase (GSK)-3β as the major kinase hub in MASH. GSK3β-activating phosphorylation was increased in primary human LSECs treated with the toxic lipid palmitate and in human MASH. Palmitate upregulated the expression of C-X-C motif chemokine ligand 2, intracellular adhesion molecule 1, and phosphorylated focal adhesion kinase, via a GSK3-dependent mechanism. Congruently, the adhesive and transendothelial migratory capacities of primary human neutrophils and THP-1 monocytes through the LSEC monolayer under lipotoxic stress were reduced by GSK3 inhibition. Treatment with the GSK3 inhibitors LY2090314 and elraglusib ameliorated liver inflammation, injury, and fibrosis in FFC- and CDHFD-fed mice, respectively. Immunophenotyping using cytometry by mass cytometry by time of flight of intrahepatic leukocytes from CDHFD-fed mice treated with elraglusib showed reduced infiltration of proinflammatory monocyte-derived macrophages and monocyte-derived dendritic cells.

Conclusion:

GSK3 inhibition attenuates lipotoxicity-induced LSEC endotheliopathy and could serve as a potential therapeutic strategy for treating human MASH.

Impact and Implications:

LSECs under lipotoxic stress in MASH develop a proinflammatory phenotype known as endotheliopathy, with obscure mediators and functional outcomes. The current study identified GSK3 as the major driver of LSEC endotheliopathy, examined its pathogenic role in myeloid cell-associated liver inflammation, and defined the therapeutic efficacy of pharmacological GSK3 inhibitors in murine MASH. This study provides preclinical data for the future investigation of GSK3 pharmacological inhibitors in human MASH. The results of this study are important to hepatologists, vascular biologists, and investigators studying the mechanisms of inflammatory liver disease and MASH, as well as those interested in drug development.

News (Medical) associated with Elraglusib

08 Jan 2025

·www.pharmaceutical-technology.com

EMA gives OMPD to Actuate’s pancreatic cancer therapy

Elraglusib is aimed at treating pancreatic ductal adenocarcinoma. Credit: Jo Panuwat D/Shutterstock. Actuate Therapeutics has gained orphan medicinal product designation (OMPD) from the European Medicines Agency (EMA) for elraglusib to treat pancreatic ductal adenocarcinoma (PDAC). The glycogen synthase kinase-3 beta (GSK-3β) inhibitor elraglusib is being studied as a first-line therapy in combination with gemcitabine/nab-paclitaxel (GnP) in individuals with metastatic pancreatic cancer (mPDAC). The randomised Actuate-1801 Part 3β trial is comparing this combination to GnP alone. The Phase II trial’s interim analysis revealed a one-year survival rate increase with a p-value of 0.002 and a median overall survival with a hazard ratio of 0.63 and a p-value of 0.016, favouring the elraglusib combination. Actuate Therapeutics CEO and president Daniel Schmitt stated: “This regulatory milestone, along with the recently announced positive interim results from our Phase II trial of elraglusib in patients with mPDAC that showed a significant clinical benefit and anti-tumour activity, should expedite our efforts to advance elraglusib as a novel, potential treatment for mPDAC. “We look forward to reporting topline data from our Phase II trial in 1H 2025 and working closely with the EMA and the FDA [US Food and Drugs Administration] to accelerate elraglusib’s clinical development programme in metastatic pancreatic cancer.” Elraglusib, the company’s lead investigational candidate, targets molecular pathways that promote tumour growth and resistance to conventional cancer treatments, including several DNA damage response (DDR) pathways. It is tailored to mediate anti-tumour immunity by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and regulating several immune checkpoints and immune cell functions. EMA orphan designation is awarded to therapies for life-threatening or chronically debilitating diseases that affect no more than two in 10,000 individuals in the European Union (EU) and for which there is no satisfactory therapy.

Clinical ResultOrphan DrugPhase 2Immunotherapy

07 Jan 2025

·www.globenewswire.com

Actuate Therapeutics Receives EMA Orphan Medicinal Product Designation for Elraglusib for the Treatment of Pancreatic Cancer

CHICAGO and FORT WORTH, Texas, Jan. 07, 2025 (GLOBE NEWSWIRE) -- Actuate Therapeutics, Inc. (NASDAQ: ACTU) (“Actuate” or the “Company”), a clinical-stage biopharmaceutical company focused on developing therapies for the treatment of high-impact, difficult-to-treat cancers through the inhibition of glycogen synthase kinase-3 beta (GSK-3β), today announced that the European Medicines Agency (EMA) has granted Orphan Medicinal Product Designation (OMPD) to elraglusib, a novel GSK-3β inhibitor, for the treatment of pancreatic ductal adenocarcinoma (PDAC). “With limited treatment options available for patients with PDAC, the EMA Orphan Drug Designation and FDA Orphan Drug Designation granted to elraglusib for the same indication reflect elraglusib’s potential to address a critical need for people living with this aggressive disease with a notably poor prognosis. This regulatory milestone, along with the recently announced positive interim results from our Phase 2 trial of elraglusib in patients with mPDAC that showed a significant clinical benefit and anti-tumor activity, should expedite our efforts to advance elraglusib as a novel, potential treatment for mPDAC,” said Daniel Schmitt, President & Chief Executive Officer of Actuate. “We look forward to reporting topline data from our Phase 2 trial in 1H 2025 and working closely with the EMA and the FDA to accelerate elraglusib’s clinical development program in metastatic pancreatic cancer.” Elraglusib is a novel GSK-3β inhibitor currently in a randomized Phase 2 trial (Actuate-1801 Part 3B study, NCT03678883) comparing the combination of elraglusib with gemcitabine/nab-paclitaxel (GnP) to GnP alone as a first line therapy in patients with metastatic pancreatic cancer (mPDAC). A recently reported analysis of interim Phase 2 data demonstrated that treatment with the elraglusib combination led to statistically significant increases in 1-year survival rate (p value of 0.002) and median overall survival (hazard ratio of 0.63, p value of 0.016) versus treatment with GnP alone. Orphan Designation is granted to therapies intended for the treatment, prevention, or diagnosis of life-threatening or chronically debilitating diseases that affect no more than two in 10,000 people in the European Union (EU) and for which no satisfactory therapy is available. The treatment must also provide significant benefit to those affected by the condition. EMA orphan drug designation provides certain benefits, including the potential for 10 years of market exclusivity following regulatory approval in the EU, reduction in regulatory fees and a centralized EU approval process1. 1. European Medicines Agency, "Orphan Designation." https://www.ema.europa.eu/en/human-regulatory-overview/orphan-designation-overview About Actuate Therapeutics, Inc. Actuate is a clinical-stage biopharmaceutical company focused on developing therapies for the treatment of high-impact, difficult-to-treat cancers. Actuate’s lead investigational drug product, elraglusib (a novel GSK-3β inhibitor), targets molecular pathways in cancer that are involved in promoting tumor growth and resistance to conventional cancer drugs such as chemotherapy including several DNA Damage Response (DDR) pathways. Elraglusib is designed to act as a mediator of anti-tumor immunity through the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and regulates multiple immune checkpoints and immune cell function. For additional information, please visit the Company’s website at http://www.actuatetherapeutics.com. Forward-Looking Statements This press release contains forward-looking statements about us, including our clinical trials and development plans, and our industry. The words “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “might,” “ongoing,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” “would,” or the negative of these terms or other comparable terminology are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. All statements, other than statements related to present facts or current conditions or of historical facts, contained in this press release are forward-looking statements. Accordingly, these statements involve estimates, assumptions, substantial risks and uncertainties which could cause actual results to differ materially from those expressed in them, including but not limited to that clinical and preclinical drug development involves a lengthy and expensive process with uncertain timelines and outcomes, results of prior preclinical studies and early clinical trials are not necessarily predictive of future results, and elraglusib may not achieve positive clinical results or favorable preclinical results or receive regulatory approval on a timely basis, if at all; that we may not successfully enroll additional patients or establish or advance plans for further development, including through conversations with the FDA or EMA and the standards such bodies may impose for such development; that elraglusib could be associated with side effects, adverse events or other properties or safety risks, which could delay or preclude regulatory approval, cause us to suspend or discontinue clinical trials or result in other negative consequences; preliminary and unpublished data may be subject to change following the availability of more data or following a more comprehensive review of the data and should not be relied upon as a final analysis; our reliance on third parties to conduct our non-clinical studies and our clinical trials; our reliance on third-party licensors and ability to preserve and protect our intellectual property rights; that we face significant competition from other biotechnology and pharmaceutical companies; our ability to fund development activities; and our ability to realize any benefits or value associated with the Orphan Medicinal Product Designation (OMPD) granted to elraglusib by the EMA for the treatment of pancreatic ductal adenocarcinoma (PDAC). In addition, any forward-looking statements are qualified in their entirety by reference to the factors discussed under the heading “Item 1A. Risk Factors” in our Quarterly Report on Form 10-Q for the quarter ended September 30, 2024 filed with the SEC on November 13, 2024 and other filings with the SEC. Because the risk factors referred to above could cause actual results or outcomes to differ materially from those expressed in any forward-looking statements made by us or on our behalf, you should not place undue reliance on any forward-looking statements. Further, any forward-looking statement speaks only as of the date on which it is made. New factors emerge from time to time, and it is not possible for us to predict which factors will arise. In addition, we cannot assess the impact of each factor on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements. Unless legally required, we do not undertake any obligation to release publicly any revisions to such forward-looking statements to reflect events or circumstances after the date of this press release or to reflect the occurrence of unanticipated events. Investor Contact Mike MoyerManaging DirectorLifeSci Advisors, LLCmmoyer@lifesciadvisors.com

Orphan DrugClinical ResultPhase 2

17 Dec 2024

·pipelinereview.com

Actuate Therapeutics Announces Positive Interim Phase 2 Data of Elraglusib in First Line Treatment of Metastatic Pancreatic Cancer

CHICAGO, IL and FORT WORTH, TX, USA I December 17, 2024 I Actuate Therapeutics, Inc. (NASDAQ: ACTU) (“Actuate” or the “Company”), a clinical-stage biopharmaceutical company focused on developing therapies for the treatment of high-impact, difficult-to-treat cancers through the inhibition of glycogen synthase kinase-3 beta (GSK-3β), today announced new positive data from its ongoing and fully enrolled randomized Phase 2 trial of elraglusib in combination with gemcitabine/nab-paclitaxel (GnP) in first line treatment of metastatic pancreatic ductal adenocarcinoma (mPDAC) (Actuate-1801 Part 3B). A pre-specified analysis was triggered by reaching >70% death events in the GnP control arm (data cut off November 15, 2024). The analysis of interim data demonstrated treatment with elraglusib in combination with GnP resulted in statistically significant increases in 1-year survival rate (p value of 0.002) and median overall survival (p value of 0.016, hazard ratio of 0.63) versus treatment with GnP alone. The combination treatment also resulted in increased Objective Response Rates (ORR) and Disease Control Rates (DCR) in the elraglusib/GnP combination arm versus the GnP control arm. “These interim results are highly encouraging and underscore the transformative potential of elraglusib in the treatment of metastatic pancreatic cancer,” said Daniel Schmitt, President & Chief Executive Officer of Actuate. “The improvement in median and overall long-term survival, disease control rate and overall response rate compared to GnP alone, combined with elraglusib’s favorable risk-benefit profile, offers the possibility of improved outcomes for patients with limited treatment alternatives. We are excited to continue evaluating the potential of elraglusib, a novel immune-oncology GSK-3 targeted approach for mPDAC, and look forward to engaging with the FDA in 1H 2025 to share topline data and discuss next steps, including a proposed phase 3 registration trial.” Inhibition of GSK-3β may inhibit tumor growth and improve survival through several complimentary mechanisms that include enhancement of chemotherapy activity, activation of innate anti-tumor immunity and regulation of gene expression, leading to alterations in tumor metabolism and Epithelial-to-Mesenchymal Transition (EMT). Study highlights include: “Pancreatic cancer is one of the most aggressive and lethal cancers with less than 5% survival rate in the US at 5 years. We are encouraged by consistent evidence of significant clinical benefit and anti-tumor activity in the elraglusib combination arm across multiple endpoints in this study,” said Dr. Andrew Mazar, Actuate’s Scientific Co-Founder and Chief Operating Officer. “Further, the favorable risk-benefit profile observed to date may provide a treatment option for many patients with metastatic pancreatic cancer that may not tolerate more aggressive and less tolerable chemotherapy approaches.” The ongoing Actuate-1801 Part 3B study (NCT04239092) is a randomized, controlled Phase 2 trial of elraglusib with GnP versus GnP alone in first line mPDAC. The trial enrolled 286 mPDAC patients with no prior systemic treatment for metastatic disease, who were randomized 2:1 to the elraglusib treatment arm (elraglusib + GnP) or the control arm (GnP alone). Elraglusib is administered at a dose of 9.3 mg/kg by IV infusion on Day 1 of each week of a 28-day cycle. The primary endpoint is 1-year survival rate, with mOS the primary parameter for summarization of survival data at the end of the study. Secondary endpoints are DCR, ORR, PFS and AE. About Actuate Therapeutics, Inc. Actuate is a clinical-stage biopharmaceutical company focused on developing therapies for the treatment of high-impact, difficult-to-treat cancers. Actuate’s lead investigational drug product, elraglusib (a novel GSK-3β inhibitor), targets molecular pathways in cancer that are involved in promoting tumor growth and resistance to conventional cancer drugs such as chemotherapy including several DNA Damage Response (DDR) pathways. Elraglusib is designed to act as a mediator of anti-tumor immunity through the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and regulates multiple immune checkpoints and immune cell function. For additional information, please visit the Company’s website at http://www.actuatetherapeutics.com. SOURCE : Actuate Therapeutics

Clinical ResultPhase 2Phase 3Immunotherapy

100 Deals associated with Elraglusib

External Link

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB16047

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Metastatic melanoma	Phase 2	US	Actuate Therapeutics, Inc.Startup	31 May 2023
Metastatic melanoma	Phase 2	US	Lantern Pharma, Inc.	31 May 2023
Metastatic Pancreatic Cancer	Phase 2	US	Actuate Therapeutics, Inc.Startup	21 Mar 2022
Pancreatic adenocarcinoma metastatic	Phase 2	US	Actuate Therapeutics, Inc.Startup	21 Mar 2022
Ewing Sarcoma	Phase 2	US	Actuate Therapeutics, Inc.Startup	01 Mar 2022
Metastatic osteosarcoma	Phase 2	US	Actuate Therapeutics, Inc.Startup	01 Mar 2022
Advanced Pancreatic Adenocarcinoma	Phase 2	US	Actuate Therapeutics, Inc.Startup	26 Jan 2022
Advanced Pancreatic Adenocarcinoma	Phase 2	US	Incyte Corp.	26 Jan 2022
Pancreatic Ductal Adenocarcinoma	Phase 2	US	Actuate Therapeutics, Inc.Startup	26 Jan 2022
Pancreatic Ductal Adenocarcinoma	Phase 2	US	Incyte Corp.	26 Jan 2022

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04239092 (Actuate-1801, GlobeNewswire) Manual	Phase 2	Pancreatic Cancer First line	286	Elraglusib + gemcitabine/nab-paclitaxel	jnblvuxzxg(bevdeziqim) = eztqtjupmz svsayvdtxt (oxdstmrmzb ) Met View more	Positive	17 Dec 2024
NCT04239092 (Actuate-1801, GlobeNewswire) Manual	Phase 2	Pancreatic Cancer First line	286	gemcitabine/nab-paclitaxel	jnblvuxzxg(bevdeziqim) = anehkvuqbl svsayvdtxt (oxdstmrmzb ) Met View more	Positive	17 Dec 2024
NCT03678883 (ASCO 12023 \| ASCO 22023) Manual	Phase 2	Advanced Pancreatic Ductal Adenocarcinoma	42	gemcitabine+Albumin-Bound Paclitaxel+Elraglusib	iwewdcrvud(iqhekbhouq) = skcorhyvic vldyvwxnyf (vmuaurupfs, 32.5 - 70.6) View more	Positive	26 May 2023
NCT03678883 (AACR2023) Manual	Phase 1/2	Advanced cancer Third line	-	elraglusib (melanoma)	jqabrfltwg(ujiekervve) = fdgbzofkvj gxurmxoots (jyniifsnbf )	Positive	14 Apr 2023
NCT03678883 (AACR2023) Manual	Phase 1/2	Advanced cancer Third line	-	elraglusib (colorectal cancer)	cjnwvvnqrb(rhbhimtist) = giuzpaszje cuedhftehm (bmzkdciiuh ) View more	Positive	14 Apr 2023
NCT04239092 (ASCO2022) Manual	Phase 1/2	Neoplasms	23	ElraglusibElraglusib alone or in combination with chemotherapy	ixqikyrkmo(nabzqrzjqv) = none rfxpqzawgw (smcdhfhczd ) View more	Positive	02 Jun 2022
NCT04239092 (ASCO2022) Manual	Phase 1/2	Neoplasms	23	Elraglusib + cyclophosphamide/topotecan or irinotecan		Positive	02 Jun 2022
NCT03678883 (Pubmed) Manual	Phase 1/2	Neoplasms \| Malignant glioma of brain	18	Lomustine+Elraglusib	vhszpndjuq(dhggvdvkun) = mild vision changes 50%, infusion reactions 22% hhkbpmtqmz (zyddggkrma ) View more	Positive	07 Feb 2022
NCT03678883 (ACTUATE 1801, SNO2021)	Phase 1/2	Glioma IDH \| 1p19q \| MGMT ... View more	18	9-ING-41 monotherapy	shgefgbohe(vcgruouosf) = ueptplcony lxhcvdksbq (tpoiobfhlo ) View more	Positive	12 Nov 2021
NCT03678883 (ACTUATE 1801, SNO2021)	Phase 1/2	Glioma IDH \| 1p19q \| MGMT ... View more	18	9-ING-41 + Lomustine	gdvsfongtx(mcorojucwu) = yclnracswt xlwbuwbpux (rfkuuahygb ) View more	Positive	12 Nov 2021
AACR2021	Not Applicable	Colorectal Cancer	-	9-ING-41	xpmrosdhob(bxfaohescz) = nrhflkhgqz utuspfwkez (ipjbbieyxt ) View more	-	01 Jul 2021
NCT03678883 (ASCO 12021 \| ASCO 22021) Manual	Phase 1/2	Solid tumor \| Malignant glioma of brain \| Refractory Hematologic Malignancy	227	lomustine+9-ing-41	wiujemwlci(pecsttmaio) = upgsrriooh mqjsnvhwtf (mhbwxyjvks ) View more	Positive	28 May 2021
NCT03678883 (ASCO2020)	Phase 1	Neoplasms	101	9-ING-41 combined with chemotherapy	chvmjioutt(fhyhrrddtk) = n = 14 zqqfdcwdwk (hjvomoqhvi ) View more	Positive	25 May 2020
NCT04218071 \| NCT03678883 \| NCT04239092 (Pubmed \| Anticancer Drugs)	Phase 1/2	Neuroblastoma	17	9-ING-41	loqjnaixhi(innjozwqzz) = cujwghghku tsvqcqnkcn (bdssddctwi )	-	01 Sep 2018

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