A Phase 3, Randomized, Double-blind, Placebo-controlled Study to Assess the Efficacy and Safety of Entospletinib in Combination With Intensive Induction and Consolidation Chemotherapy in Adults With Newly Diagnosed Nucleophosmin 1-mutated Acute Myeloid Leukemia

The primary objective of this study is to evaluate the efficacy of entospletinib (ENTO) compared to placebo when added to chemotherapy in previously untreated nucleophosmin-1 mutated (NPM1-m) acute myeloid leukemia (AML), as defined by the rate of molecularly defined measurable residual disease (MRD).

Start Date24 Nov 2021

Sponsor / Collaborator

Kronos Bio, Inc.

NCT03225924

/ TerminatedPhase 1/2IIT

Phase Ib - II Study of Entospletinib (ENTO) in Newly Diagnosed Diffuse Large B Cell Lymphoma (DLBCL) Patients With aaIPI>=1 Treated by Rituximab, Cyclophosphamide, Hydroxydaunomycin, Oncovin, and Prednisone (R-CHOP)

The primary objective of the phase Ib of the study is to determine the recommended phase 2 dose (RP2D) for entospletinib (ENTO) in patients treated with R-CHOP.
The primary objective of the phase II is to determine the complete metabolic response (CMR) rate by the Lugano classification 2014 (Deauville scale 1-3) at the end of treatment.

Start Date26 Jul 2017

Sponsor / Collaborator

Le LYSARC

NCT03010358

/ CompletedPhase 1/2IIT

A Phase I/II Study of Syk Inhibitor Entospletinib (GS-9973) in Combination With Obinutuzumab in Patients With Relapsed/Refractory Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL) and B-Cell Malignancies

This phase I/II trial studies the side effect and best dose of entospletinib when giving together with obinutuzumab and to see how well they work in treating patients with chronic lymphocytic leukemia, small lymphocytic lymphoma, or non-Hodgkin lymphoma that has come back. Entospletinib may stop the growth of cancer cells by blocking some of the enzymes need for cell growth. Monoclonal antibodies, such as obinutuzumab, may interfere with the ability of cancer cells to grow and spread. Giving entospletinib and obinutuzumab together may work better in treating patients with chronic lymphocytic leukemia, small lymphocytic lymphoma, or non-Hodgkin lymphoma.

Start Date17 Jul 2017

Sponsor / Collaborator

OHSU Knight Cancer Institute

[+2]

100 Clinical Results associated with Entospletinib Dimesylate

100 Translational Medicine associated with Entospletinib Dimesylate

100 Patents (Medical) associated with Entospletinib Dimesylate

130

Literatures (Medical) associated with Entospletinib Dimesylate

01 Mar 2025·Hematological Oncology

Gene Expression Profiling in Acute Myeloid Leukemia Patient Subgroups With High and Low Sensitivity Toward SYK Inhibitors

Article

Author: Brattås, Marte Karen ; Görtler, Franziska ; Johansen, Silje ; Hatfield, Kimberley Joanne ; Rye, Kristin Paulsen ; Reikvam, Håkon

ABSTRACTAcute myeloid leukemia (AML) is a heterogeneous malignancy characterized by the uncontrolled proliferation of myeloid cells, and despite recent treatment advances, patient outcomes remain suboptimal. The cytoplasmic spleen tyrosine kinase (SYK) has emerged as a promising therapeutic target in AML due to its role in promoting leukemic cell survival, proliferation, and chemoresistance. This study investigates in vitro antiproliferative effects of SYK inhibitors on leukemia cells by analyzing 48 primary AML samples treated with five SYK inhibitors: fostamatinib, entospletinib, cerdulatinib, TAK‐659, and RO9021. Our findings revealed significant heterogeneity among patients, leading to the identification of two distinct patient sample groups that were identified as having either high or low sensitivity toward SYK inhibitors. Furthermore, gene expression profiling through RNA sequencing of AML patient samples uncovered 97 significantly differentially expressed genes (DEGs) between the two patient groups with high or low in vitro sensitivity toward SYK inhibitors. Pathway enrichment analyses revealed that the high‐sensitivity group was enriched in biological processes related to positive gene regulation and significant pathways included cell adhesion molecules and proteoglycans. In contrast, the low‐sensitivity group showed enrichment in pathways related to PI3K‐Akt signaling and JAK‐STAT signaling.Gene set enrichment analysis further highlighted that high‐sensitivity patient samples were upregulated in pathways associated with oxidative phosphorylation and MYC targets, whereas low‐sensitivity patient samples showed enrichment in TGF beta signaling and IL6 JAK STAT3 signaling. These results identify gene expression profile signatures that may predict sensitivity to SYK inhibition and underscore the potential for personalized therapeutic strategies in AML.

01 Oct 2024·Environmental Toxicology

Exploring the impact of ITGB2 on glioma progression and treatment: Insights from non‐apoptotic cell death and immunotherapy

Article

Author: Xia, Ying ; Liu, Chao ; Peng, Jun ; Hu, Linwang ; Chen, Zigui ; Zeng, Biying ; Zhuang, Junhong ; Miao, Changfeng

AbstractIn the realm of glioma treatment, our groundbreaking research has uncovered the pivotal role of Integrin Beta 2 (ITGB2) in non‐apoptotic cell death and its profound implications for immunotherapy efficacy. Gliomas, known for their aggressive and infiltrative nature, demand innovative therapeutic strategies for improved patient outcomes. Our study bridges a critical gap by examining the interplay between non‐apoptotic cell death and immunotherapy response in gliomas. Through comprehensive analysis of ten diverse glioma datasets, we developed a unique death enrichment score and identified ITGB2 as a significant risk marker. This study demonstrates that ITGB2 can predict immune activity, mutation characteristics, and drug response in glioma patients. We reveal that ITGB2 not only mediates glioma proliferation and migration but also crucially influences immunotherapy responses by modulating the interaction between gliomas and macrophages by single‐cell sequencing analysis (iTalk and ICELLNET). Employing a variety of molecular and cellular methodologies, including in vitro models, our findings highlight ITGB2 as a potent marker in glioma biology, particularly impacting macrophage migration and polarization. We present compelling evidence of ITGB2's dual role in regulating tumor cell behavior and shaping the immune landscape, thereby influencing therapeutic outcomes. The study underlines the potential of ITGB2‐targeted strategies in enhancing the efficacy of immunotherapy and opens new avenues for personalized treatment approaches in glioma management. In conclusion, this research marks a significant stride in understanding glioma pathology and therapy, positioning ITGB2 as a key biomarker and a promising target in the quest for effective glioma treatments.

01 Sep 2024·Cardiovascular Pathology

A pathological study on the efficacy of Syk inhibitors in a Candida albicans-induced aortic root vasculitis murine model

Article

Author: Takahashi, Kei ; Yokouchi, Yuki ; Ohno, Naohito ; Miura, Noriko ; Asakawa, Nanae ; Oharaseki, Toshiaki

BACKGROUNDThe activation of innate immunity may be involved in the development of Candida albicans-induced murine vasculitis, which resembles Kawasaki disease (KD) vasculitis. This study aimed to histologically clarify the time course of the development of vasculitis in this model in detail and to estimate the potential role of spleen tyrosine kinase (Syk) inhibitors in KD vasculitis.METHODS AND RESULTSDBA/2 male mice were intraperitoneally injected with a vasculitis-inducing substance and treated with a Syk inhibitor (R788 or GS-9973). Systemic vasculitis, especially in the aortic annulus area, was histologically evaluated. Regarding lesions in the aortic annulus area, some mice in the untreated control group already showed initiation of vasculitis 1 day after the final injection of a vasculitis-inducing substance. The vasculitis expanded over time. Inflammation occurred more frequently at the aortic root than at the coronary artery. The distribution of inflammatory cells was limited to the intima, intima plus adventitia, or all layers. In the Syk inhibitor-treated groups, only one mouse had vasculitis at all observation periods. The severity and area of the vasculitis were reduced by both Syk inhibitors.CONCLUSIONCandida albicans-induced murine vasculitis may occur within 1 day after the injection of a vasculitis-inducing substance. Additionally, Syk inhibitors suppress murine vasculitis.

News (Medical) associated with Entospletinib Dimesylate

01 May 2025

·www.globenewswire.com

Kronos Bio Enters into Agreement to Be Acquired by Concentra Biosciences for $0.57 in Cash per Share Plus a Contingent Value Right

CAMBRIDGE, Mass., May 01, 2025 (GLOBE NEWSWIRE) -- Kronos Bio, Inc. ("Kronos Bio") (Nasdaq: KRON), a biotechnology company that has been developing small molecule therapeutics to address cancers and other diseases driven by deregulated transcription, today announced that it has entered into a definitive merger agreement (the “Merger Agreement”) with Concentra Biosciences, LLC ( “Concentra”), whereby Concentra will acquire Kronos Bio for $0.57 in cash per share of Kronos Bio common stock (“Kronos Bio Common Stock”), plus one non-tradeable contingent value right ("CVR"), which represents the right to receive: (i) 50% of the net proceeds in the case of a disposition of the Company’s product candidates known as KB-9558 and KB-7898 that occurs within 2 years following closing; (ii) 100% of the net proceeds in the case of a disposition of the Company’s product candidates known as KB-0742, lanraplenib and entospletinib that occurs prior to closing; (iii) 100% of cost savings realized prior to closing; (iv) 80% of cost savings realized between the merger closing date and the second (2nd) anniversary of the merger closing date; and (v) 50% of cost savings realized between the second (2nd) anniversary of the merger closing date and the third (3rd) anniversary of the merger closing date, each pursuant to the contingent value rights agreement (the “CVR Agreement”). Following a review process conducted with the assistance of its legal and financial advisors, the Kronos Bio Board of Directors has determined that the acquisition by Concentra is in the best interests of all Kronos Bio shareholders and has approved the Merger Agreement and related transactions. Pursuant and subject to the terms of the Merger Agreement, a wholly owned subsidiary of Concentra will commence a tender offer (the “Offer”) by May 15, 2025 to acquire all outstanding shares of Kronos Bio Common Stock. Closing of the Offer is subject to certain conditions, including the tender of Kronos Bio Common Stock representing at least a majority of the total number of outstanding shares (including any shares held by Concentra), the availability of at least $40.0 million of cash (net of transaction costs and other liabilities) at closing, and other customary closing conditions. Kronos Bio officers, directors and their respective affiliates holding approximately 27% of Kronos Bio Common Stock have signed tender and support agreements under which such parties have agreed to tender their shares in the Offer and support the merger transaction. The merger transaction is expected to close mid-2025. About Kronos BioKronos Bio is a biopharmaceutical company that has historically focused on the discovery and development of small molecule therapeutics to address deregulated transcription, a hallmark of cancer and autoimmune diseases. Kronos Bio has a research facility in Cambridge, Mass. For more information, visit https://www.kronosbio.com. AdvisorsGoodwin Procter LLP is acting as legal counsel to Kronos Bio and Leerink Partners is acting as sole financial advisor to Kronos Bio. Gibson, Dunn & Crutcher LLP is acting as legal counsel to Concentra. Forward-Looking Statements This release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including, but not limited to, statements regarding Kronos Bio’s beliefs and expectations and statements about the Offer, merger, related transactions contemplated by the Merger Agreement and the CVR Agreement (the “Transactions”), including the timing of and closing conditions to the Transactions, and the potential effects of the proposed Transactions on Kronos Bio and the potential payment of proceeds to the Kronos Bio stockholders, if any, pursuant to the CVR Agreement. These statements may be identified by their use of forward-looking terminology including, but not limited to, “anticipate,” “believe,” “continue,” “could,” “estimate,” “expect,” “goal,” “intend,” “may,” “might,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” and “would,” and similar words expressions are intended to identify forward-looking statements. Forward-looking statements are neither historical facts nor assurances of future performance and involve risks and uncertainties that could cause actual results to differ materially from those projected, expressed or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: the possibility that various closing conditions set forth in the Merger Agreement may not be satisfied or waived, including uncertainties as to the percentage of Kronos Bio’s stockholders tendering their shares in the Offer; the possibility that competing offers will be made; the risk that the Transactions may not be completed in a timely manner, or at all, which may adversely affect Kronos Bio’s business and the price of its common stock; costs associated with the proposed Transactions; the risk that any stockholder litigation in connection with the Transactions may result in significant costs of defense, indemnification and liability; the risk that activities related to the CVR Agreement may not result in any value to the Kronos Bio stockholders; and other risks and uncertainties discussed in Kronos Bio’s most recent annual report filed with the Securities and Exchange Commission (the “SEC”) as well as in Kronos Bio’s subsequent filings with the SEC. As a result of such risks and uncertainties, Kronos Bio’s actual results may differ materially from any future results, performance or achievements discussed in or implied by the forward-looking statements contained herein. There can be no assurance that the proposed Transactions will in fact be consummated. Kronos Bio cautions investors not to unduly rely on any forward-looking statements. The forward-looking statements contained in this release are made as of the date hereof, and Kronos Bio undertakes no obligation to update any forward-looking statements, whether as a result of future events, new information or otherwise, except as expressly required by law. All forward-looking statements in this document are qualified in their entirety by this cautionary statement. Additional Information and Where to Find It The Offer described in this release has not yet commenced, and this release is neither a recommendation, nor an offer to purchase nor a solicitation of an offer to sell any shares of the common stock of Kronos Bio or any other securities. On the commencement date of the Offer, a tender offer statement on Schedule TO, including an offer to purchase, a letter of transmittal and related documents, will be filed with the SEC by Concentra and its acquisition subsidiary, and a Solicitation/Recommendation Statement on Schedule 14D-9 will be filed with the SEC by Kronos Bio. The Offer to purchase the outstanding shares of the common stock of Kronos Bio will only be made pursuant to the offer to purchase, the letter of transmittal and related documents filed as a part of the Schedule TO. INVESTORS AND SECURITY HOLDERS ARE URGED TO READ THE TENDER OFFER MATERIALS (INCLUDING THE OFFER TO PURCHASE, A LETTER OF TRANSMITTAL AND RELATED DOCUMENTS) AND THE SOLICITATION/RECOMMENDATION STATEMENT ON SCHEDULE 14D-9 REGARDING THE OFFER, AS THEY MAY BE AMENDED OR SUPPLEMENTED FROM TIME TO TIME, WHEN THEY BECOME AVAILABLE BECAUSE THEY WILL CONTAIN IMPORTANT INFORMATION THAT INVESTORS AND SECURITY HOLDERS SHOULD CONSIDER BEFORE MAKING ANY DECISION REGARDING TENDERING THEIR SHARES, INCLUDING THE TERMS AND CONDITIONS OF THE OFFER. Investors and security holders may obtain a free copy of these statements (when available) and other documents filed with the SEC at the website maintained by the SEC at www.sec.gov or by directing such requests to the information agent for the Offer, which will be named in the tender offer statement. Investors and security holders may also obtain, at no charge, the documents filed or furnished to the SEC by Kronos Bio under the “Investors & Media” section of Kronos Bio’s website at https://ir.kronosbio.com/financials-filings/sec-filings. Contact Information: Investors: Denise Powell denise@redhousecomms.com Media: Kelli Perkins kelli@redhousecomms.com

Acquisition

25 Jan 2024

·www.fiercebiotech.com

Kronos calls time on CMO, CSO roles as part of C-suite shakeup

Replacing the three jettisoned C-suite roles will be four SPV positions overseeing: R&D; clinical development; corporate strategy and portfolio management; and corporate operations and legal. Kronos Bio had already trimmed back its headcount and pipeline in the wake of a mid-stage cancer flop. Now, it’s the company’s C-suite who are heading to the exits. The biotech has “eliminated three executive officer roles”—meaning Chief Medical Officer Jorge DiMartino, M.D., Chief Scientific Officer Christopher Dinsmore, Ph.D., and Chief Operating Officer and General Counsel Barbara Kosacz will all be out of a job. The company explained the changes were needed to ensure a “streamlined leadership structure designed to focus on pipeline advancement and align with Kronos Bio’s current operating needs.” The three executives will leave the company on Feb.16, although they will remain as strategic advisors for the business, according to a Jan. 25 press release. The leadership shakeup follows a headcount reduction of 19% in November in order to fund KB-0742, a CDK9 inhibitor currently in a phase 1/2 trial for solid tumors and non-Hodgkin lymphoma. A month after the layoffs, Kronos said it was discontinuing a cancer trial for lanraplenib and seeking a partner for the SYK inhibitor in the wake of a mid-stage trial flop. “This new leadership structure is designed to streamline our operations and reflects our ongoing effort to advance our pipeline, optimize our resources, and efficiently deliver on our business objectives,” CEO Norbert Bischofberger, Ph.D., said in the release. “I would like to thank Jorge, Chris, and Barbara for their leadership and dedication, and I wish them well in their future endeavors,” Bischofberger added. “They each built and managed strong teams, laying the groundwork for this new structure and preparing our future leaders for success.” Replacing the three jettisoned C-suite roles will be four SPV positions overseeing R&D; clinical development; corporate strategy and portfolio management; and corporate operations and legal. Those positions are filled by Charles Lin, Ph.D., Elizabeth Olek, Rocio Martin Hoyos and Allison Frisbee, respectively. Kronos said it expects to make savings from the changes, even after termination costs are accounted for. Besides KB-0742, Kronos has a partnership with Roche’s Genentech for several undisclosed discovery programs. Inked a year ago, the Genentech partnership is crucial for Kronos, coming right after the biotech kicked a late-stage AML asset called entospletinib to the curb. The Roche unit jumped in to save the day for the struggling biotech with a $20 million upfront payment plus milestones that could top $177 million for the first program and $100 million for the first licensed product. Kronos also recently revealed a new development candidate, dubbed KB-9558. The preclinical asset is designed to modulate the IRF4 transcription regulatory network—a key driver in multiple myeloma.

Executive Change

28 Dec 2023

·synapse.patsnap.com

What are Syk inhibitors and how do you quickly get the latest development progress?

Syk (Spleen Tyrosine Kinase) is a crucial enzyme found in the human body that plays a significant role in immune cell signaling. It is primarily expressed in cells of the hematopoietic system, such as B cells, T cells, and mast cells. Syk acts as a key mediator in various immune responses, including B cell receptor signaling, Fc receptor signaling, and integrin signaling. By initiating downstream signaling cascades, Syk regulates immune cell activation, differentiation, and cytokine production. Due to its pivotal role in immune cell function, Syk has emerged as a potential therapeutic target for various immune-related disorders, including autoimmune diseases and certain cancers. The analysis of the current competitive landscape and future development of target Syk reveals that Rigel Pharmaceuticals, Inc., Novartis AG, HUTCHMED (China) Ltd., and TopiVert Ltd. are among the companies growing fastest under this target. These companies have made significant progress in the R&D of drugs targeting Syk, with drugs in the Approved and Phase 3 stages. Drugs targeting Syk have been approved for various indications, covering a wide range of diseases and conditions. Small molecule drugs are progressing most rapidly, indicating their potential as therapeutic options. The development of drugs targeting Syk is taking place in various countries/locations, with the United States, European Union, and China being prominent players. Further research and development are needed to fully explore the potential of drugs targeting Syk and address the inactive drugs in the pipeline. How do they work?Syk inhibitors are a type of medication that target and inhibit the activity of the spleen tyrosine kinase (Syk) enzyme. From a biomedical perspective, Syk is an enzyme involved in signaling pathways within immune cells, particularly B cells and mast cells. It plays a crucial role in the activation of these cells and the release of inflammatory mediators. Syk inhibitors work by binding to the Syk enzyme and blocking its activity. By inhibiting Syk, these medications can help regulate immune responses and reduce inflammation. They are primarily used in the treatment of certain autoimmune diseases, such as rheumatoid arthritis and immune thrombocytopenic purpura. These inhibitors are considered targeted therapies as they specifically target the Syk enzyme, minimizing potential side effects on other cellular processes. They can be administered orally or intravenously, depending on the specific medication. Syk inhibitors have shown promising results in clinical trials and are an active area of research in the field of biomedicine. List of Syk InhibitorsThe currently marketed Syk inhibitors include: Fostamatinib DisodiumMidostaurinSovleplenibIMG-016TOP-1630CerdulatinibEntospletinib DimesylateGusacitinibIC-265IC-270For more information, please click on the image below. What are Syk inhibitors used for?Syk inhibitors are primarily used in the treatment of certain autoimmune diseases, such as rheumatoid arthritis and immune thrombocytopenic purpura. For more information, please click on the image below to log in and search. How to obtain the latest development progress of Syk inhibitors?In the Synapse database, you can keep abreast of the latest research and development advances of Syk inhibitors anywhere and anytime, daily or weekly, through the "Set Alert" function. Click on the image below to embark on a brand new journey of drug discovery!

100 Deals associated with Entospletinib Dimesylate

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KEGG	Wiki	ATC	Drug Bank
-	Entospletinib Dimesylate	-	DB12121

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Acute myeloid leukemia with mutated NPM1	Phase 3	Canada	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	Spain	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	Italy	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	Czechia	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	Poland	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	Brazil	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	United States	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	France	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	South Korea	Kronos Bio, Inc.	24 Nov 2021
Acute myeloid leukemia with mutated NPM1	Phase 3	Israel	Kronos Bio, Inc.	24 Nov 2021

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05020665 (CTgov)	Phase 3	Acute myeloid leukemia with mutated NPM1	15	anthracycline+ENTO+cytarabine (ENTO)	qhheybglmo(fygvabkdjr) = ilgryllrqd qvmrrklmyg (zhmaeuujid, fzvhfjanqe - dimikyayge) View more	-	10 Jan 2024
				placebo+cytarabine (Placebo)	qhheybglmo(fygvabkdjr) = vasowhbvff qvmrrklmyg (zhmaeuujid, uuldwlozlv - gxhsdqkxpf) View more
NCT03010358 (CTgov)	Phase 1/2	Anemia \| Lymphoplasmacytic Lymphoma \| Follicular Lymphoma \| Mantle-Cell Lymphoma \| Hairy Cell Leukemia \| Recurrent Chronic Lymphoid Leukemia \| Chronic lymphocytic leukaemia refractory \| B-Cell Prolymphocytic Leukemia \| Marginal Zone B-Cell Lymphoma \| Refractory Small Lymphocytic Lymphoma \| Richter's syndrome	24	obinutuzumab+entospletinib (Phase 1, Dose 1-2)	ozxdplowva(dfnoqbhlhk) = cpzgnuduob drubdjjrqd (pjgdjfjvaw, kldkcohgui - ufbxvpdvtk)	-	08 Aug 2023
				obinutuzumab+entospletinib (All Research Participants)	jmnzrttgka(gvylehadlb) = itumasniyd jwybrvyqrn (gnjyzqojzw, fnezbgaexm - cukdhqzwef) View more
NCT03010358 (ASH 12021 \| ASH 22021) Manual	Phase 1/2	Recurrent Chronic Lymphoid Leukemia	24	Entospletinib+Obinutuzumab	(glgvuxojku) = entospletinib 400 mg twice-daily xalmsfvcnw (ibtdyzeobx )	Positive	05 Nov 2021
NCT02457598 (Pubmed \| Clin Cancer Res)	Phase 1	Chronic Lymphocytic Leukemia	53	Tirabrutinib monotherapy	(gkzhmjbphy) = wuyabuthjp nbbcsohueu (exxbwsygdb ) View more	-	15 Jun 2020
				Tirabrutinib + Idelalisib	(gkzhmjbphy) = vizvnaikxs nbbcsohueu (exxbwsygdb ) View more
NCT01796470 (CTgov)	Phase 2	Mantle-Cell Lymphoma \| Chronic Lymphocytic Leukemia \| Diffuse Large B-Cell Lymphoma \| Indolent Non-Hodgkin Lymphoma	66	Idelalisib+Entospletinib (Entospletinib + Idelalisib CLL)	brygihnfcu(bnorgsjrul) = eoggqvphdu pkpagsqnxs (mcctxzgwut, asnyxrruqg - zqtaefhnbf) View more	-	02 Jun 2020
				Idelalisib iNHL+Entospletinib (Entospletinib + Idelalisib iNHL: FL)	brygihnfcu(bnorgsjrul) = jthpqqctkp pkpagsqnxs (mcctxzgwut, peeduujgck - gfnitaxyvl) View more
NCT03135028 (Japanese AML, CTgov)	Phase 1	Acute Myeloid Leukemia	9	ENTO	qcmgnfdmag(ykphcthwho) = bzlceeiwef eukobiiuqa (thlrscxyer, tiyjyjncwy - htslmnyebh) View more	-	06 Mar 2020
NCT02983617 (CTgov)	Phase 2	Chronic Lymphocytic Leukemia	36	Tirabrutinib+Entospletinib (Tirabrutinib + Entospletinib)	zyrxkqpemo(kinnoctqil) = xdmvkqgvxz uqzxiviygz (lgkerpebda, lsodeabwzu - rrcjtyrhow) View more	-	28 Feb 2020
				Obinutuzumab+Tirabrutinib+Entospletinib (Tirabrutinib + Entospletinib + Obinutuzumab)	zyrxkqpemo(kinnoctqil) = mpnkcvvtsa uqzxiviygz (lgkerpebda, ikszgxqekt - rilpmuvnyx) View more
NCT02404220 (CTgov)	Phase 1/2	Recurrent B Acute Lymphoblastic Leukemia \| Acute Lymphoblastic Leukemia	30	CNS Prophylaxis+Dexamethasone+Vincristine+Entospletinib (ENTO 200 mg + VCR 0.5 mg)	xpselewhwa(qvvrhgrqkp) = xfhsegsbrf mhyqjsljin (fbmkzaefrx, dcbxeyvunv - qrtdudiaty) View more	-	02 Dec 2019
				CNS Prophylaxis+Dexamethasone+Vincristine+Entospletinib (ENTO 400 mg + VCR 0.5 mg)	xpselewhwa(qvvrhgrqkp) = bqrpnonvwp mhyqjsljin (fbmkzaefrx, zxzprdrfby - dtrdplakwk) View more
NCT02983617 (ASH 12019 \| ASH 22019) Manual	Phase 2	Chronic Lymphocytic Leukemia	36	Tirabrutinib+Entospletinib+Obinutuzumab	(jillhgnoyy) = tahmupexxi xkwmtbpmov (ajdjukmcez, 1.2 - 19.5) View more	Positive	13 Nov 2019
				Tirabrutinib+Entospletinib	(jillhgnoyy) = mkxyxxnbzx xkwmtbpmov (ajdjukmcez, 0 - 39.3) View more
NCT01799889 (Pubmed \| Leukemia) Manual	Phase 2	Recurrent Chronic Lymphoid Leukemia	49	Entospletinib	(sxojhxyczs) = doybkvsrty adthhyfnxa (tevstfnnzf, 3.7 - 8.3) View more	Positive	01 Aug 2019

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