Delving into the Latest Updates on Samus Therapeutics, Inc. with Synapse

Overview

This is a multicenter, Phase 2a, randomized, double-blind, placebo-controlled pilot study to assess the biological activity, safety and pharmacokinetics of PU-AD compared to placebo in ALS. It will be conducted in approximately 20 sites in the US. Approximately 30 subjects will be enrolled in this study; subjects will be randomized 3:2 to receive either PU-AD 30 mg or matching placebo qd, added onto any current stable background treatment.

Start Date01 Jan 2023

Sponsor / Collaborator

Samus Therapeutics, Inc.

NCT05612633 / WithdrawnPhase 2

A Phase 2 Open-label Study of Zelavespib (PU-H71) in Subjects With Accelerated Phase Myeloproliferative Neoplasm (AP MPN) or Blast Phase Myeloproliferative Neoplasm

This is a multicenter, Phase 2 Simon 2-Stage study designed to assess the safety, tolerability, PK, and efficacy of oral zelavespib (PU-H71) administered daily in adults with accelerated phase (10% to 19% blasts in peripheral or bone marrow) myeloproliferative neoplasm, with or without ongoing concomitant treatment with ruxolitinib.

Start Date15 Jun 2022

Sponsor / Collaborator

Samus Therapeutics, Inc.

NCT04782609 / TerminatedPhase 1

A Phase 1b Dose Escalation/Dose Expansion Study of Icapamespib (PU-AD) in Patients With Recurrent Malignant Glioma

This is a 2-part multicenter Phase 1b study designed to test icapamespib in patients with recurrent brain lesions.
Part 1 of the trial will be a standard 3 by 3 dose escalation design where different doses are examined. Part 2 will be a dose expansion cohort to further evaluate the recommended Phase 2 dose (RP2D). The RP2D is defined as the dose level recommended for further clinical study, or the highest dose tested.

Start Date27 Dec 2021

Sponsor / Collaborator

Samus Therapeutics, Inc.

100 Clinical Results associated with Samus Therapeutics, Inc.

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

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5

Literatures (Medical) associated with Samus Therapeutics, Inc.

21 Sep 2023·Blood

Epichaperome inhibition targets TP53-mutant AML and AML stem/progenitor cells

Article

Author: Nguyen, Nghi ; Martinez-Moczygemba, Margarita ; Karras, Georgios I. ; Basyal, Mahesh ; Stephan, Clifford ; Shpall, Elizabeth J. ; Muftuoglu, Muharrem ; Carter, Bing Z. ; Morgan, Robert A. ; Pemmaraju, Naveen ; Ebert, Benjamin L. ; Sobieski, Mary ; Pei, Jingqi ; Powell, Reid T. ; Ke, Baozhen ; Nishida, Yuki ; Bedoy, Andrea D. ; Mak, Po Yee ; Ostermann, Lauren B. ; Boettcher, Steffen ; Moll, Ute M. ; Andreeff, Michael ; Isgandarova, Sevinj ; Tao, Wenjing ; Wallner, Barbara

AbstractTP 53-mutant acute myeloid leukemia (AML) remains the ultimate therapeutic challenge. Epichaperomes, formed in malignant cells, consist of heat shock protein 90 (HSP90) and associated proteins that support the maturation, activity, and stability of oncogenic kinases and transcription factors including mutant p53. High-throughput drug screening identified HSP90 inhibitors as top hits in isogenic TP53–wild-type (WT) and -mutant AML cells. We detected epichaperomes in AML cells and stem/progenitor cells with TP53 mutations but not in healthy bone marrow (BM) cells. Hence, we investigated the therapeutic potential of specifically targeting epichaperomes with PU-H71 in TP53-mutant AML based on its preferred binding to HSP90 within epichaperomes. PU-H71 effectively suppressed cell intrinsic stress responses and killed AML cells, primarily by inducing apoptosis; targeted TP53-mutant stem/progenitor cells; and prolonged survival of TP53-mutant AML xenograft and patient-derived xenograft models, but it had minimal effects on healthy human BM CD34+ cells or on murine hematopoiesis. PU-H71 decreased MCL-1 and multiple signal proteins, increased proapoptotic Bcl-2-like protein 11 levels, and synergized with BCL-2 inhibitor venetoclax in TP53-mutant AML. Notably, PU-H71 effectively killed TP53-WT and -mutant cells in isogenic TP53-WT/TP53-R248W Molm13 cell mixtures, whereas MDM2 or BCL-2 inhibition only reduced TP53-WT but favored the outgrowth of TP53-mutant cells. Venetoclax enhanced the killing of both TP53-WT and -mutant cells by PU-H71 in a xenograft model. Our data suggest that epichaperome function is essential for TP53-mutant AML growth and survival and that its inhibition targets mutant AML and stem/progenitor cells, enhances venetoclax activity, and prevents the outgrowth of venetoclax-resistant TP53-mutant AML clones. These concepts warrant clinical evaluation.

15 Nov 2022·Blood

A Phase 1 Dose-Escalation Study of the Oral Epichaperome Inhibitor, Zelavespib (ZEL) in Combination with Ruxolitinib (RUX), in Patients with Relapsed Myelofibrosis: Results of the Dose Escalation Stage

Author: Snyder, Jack ; Pemmaraju, Naveen ; Verstovsek, Srdan ; Bardelli, Geraldine ; Schiller, Gary J. ; Gundabolu, Krishna ; Silverman, Michael H

15 Nov 2022·Blood

Epichaperome Inhibition Targets Kinase and TP53 Mutant Therapy Resistant AML

Author: Pemmaraju, Naveen ; Wallner, Barbara ; Andreeff, Michael ; Karras, Georgios ; Shpall, Elizabeth J ; Chiosis, Gabriela ; Mak, Po Yee ; Ostermann, Lauren B ; Morgan, Robert A ; Boettcher, Steffen ; Tao, Wenjing ; Nishida, Yuki ; Carter, Bing Z

100 Deals associated with Samus Therapeutics, Inc.

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100 Translational Medicine associated with Samus Therapeutics, Inc.

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Pipeline

Pipeline Snapshot as of 26 Nov 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

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