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

概览

疾病领域	数量

肿瘤	2
血液及淋巴系统疾病	1
免疫系统疾病	1

排名前五的药物类型	数量

小分子化药	2

关联

9

项与 Veana Therapeutics, Inc. 相关的药物

VT-101(Veana Therapeutics)

靶点-

作用机制-

在研机构

Veana Therapeutics, Inc.

原研机构

Veana Therapeutics, Inc.

在研适应症

HER2阳性乳腺癌 [+2]

非在研适应症-

最高研发阶段临床1期

首次获批国家/地区-

首次获批日期-

Alpha-Tocopheryloxyacetic acid

靶点-

作用机制

细胞凋亡刺激剂 [+1]

在研机构

Veana Therapeutics, Inc.

原研机构

Veana Therapeutics, Inc.

在研适应症

淋巴瘤 [+2]

非在研适应症

激素难治性乳腺癌 [+1]

最高研发阶段临床1期

首次获批国家/地区-

首次获批日期-

Vimo-V001

靶点-

作用机制-

在研机构-

原研机构

Veana Therapeutics, Inc.

在研适应症-

非在研适应症-

最高研发阶段无进展

首次获批国家/地区-

首次获批日期-

100 项与 Veana Therapeutics, Inc. 相关的临床结果

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0 项与 Veana Therapeutics, Inc. 相关的专利（医药）

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2

项与 Veana Therapeutics, Inc. 相关的文献（医药）

2019-12-01·Journal of Translational Medicine2区 · 医学

Blockade of TGF-β signaling to enhance the antitumor response is accompanied by dysregulation of the functional activity of CD4+CD25+Foxp3+ and CD4+CD25−Foxp3+ T cells

2区 · 医学

ArticleOA

作者: Polanczyk, Magdalena J ; Walker, Edwin ; Guerrouahen, Bella S ; Akporiaye, Emmanuel T ; Haley, Daniel

BACKGROUNDThe pleiotropic cytokine, transforming growth factor (TGF)-β, and CD4⁺CD25⁺Foxp3⁺ regulatory T cells (Tregs) play a critical role in actively suppressing antitumor immune responses. Evidence shows that TGF-β produced by tumor cells promotes tolerance via expansion of Tregs. Our group previously demonstrated that blockade of TGF-β signaling with a small molecule TGF-β receptor I antagonist (SM16) inhibited primary and metastatic tumor growth in a T cell dependent fashion. In the current study, we evaluated the effect of SM16 on Treg generation and function.METHODSUsing BALB/c, FoxP3eGFP and Rag^-/- mice, we performed FACS analysis to determine if SM16 blocked de novo TGF-β-induced Treg generation in vitro and in vivo. CD4⁺ T cells from lymph node and spleen were isolated from control mice or mice maintained on SM16 diet, and flow cytometry analysis was used to detect the frequency of CD4⁺CD25^-FoxP3⁺ and CD4⁺CD25⁺FoxP3⁺ T cells. In vitro suppression assays were used to determine the ability to suppress naive T cell proliferation in vitro of both CD4⁺CD25⁺FoxP3⁺ and CD4⁺CD25^-FoxP3⁺ T cell sub-populations. We then examined whether SM16 diet exerted an inhibitory effect on primary tumor growth and correlated with changes in FoxP3⁺expression. ELISA analysis was used to measure IFN-γ levels after 72 h co-culture of CD4⁺CD25⁺ T cells from tumor-bearing mice on control or SM16 diet with CD4⁺CD25^- T cells from naive donors.RESULTSSM16 abrogates TGF-β-induced Treg generation in vitro but does not prevent global homeostatic expansion of CD4⁺ T cell sub-populations in vivo. Instead, SM16 treatment causes expansion of a population of CD4⁺CD25^-Foxp3⁺ Treg-like cells without significantly altering the overall frequency of Treg in lymphoreplete naive and tumor-bearing mice. Importantly, both the CD4⁺CD25^-Foxp3⁺ T cells and the CD4⁺CD25⁺Foxp3⁺ Tregs in mice receiving SM16 diet exhibited diminished ability to suppress naive T cell proliferation in vitro compared to Treg from mice on control diet.CONCLUSIONSThese findings suggest that blockade of TGF-β signaling is a potentially useful strategy for blunting Treg function to enhance the anti-tumor response. Our data further suggest that the overall dampening of Treg function may involve the expansion of a quiescent Treg precursor population, which is CD4⁺CD25^-Foxp3⁺.

Frontiers in Oncology3区 · 医学

Reverting Immune Suppression to Enhance Cancer Immunotherapy

3区 · 医学

ReviewOA

作者: Rutella, Sergio ; Guerrouahen, Bella S ; Cugno, Chiara ; Maccalli, Cristina ; Akporiaye, Emmanuel T

Tumors employ strategies to escape immune control. The principle aim of most cancer immunotherapies is to restore effective immune surveillance. Among the different processes regulating immune escape, tumor microenvironment-associated soluble factors, and/or cell surface-bound molecules are mostly responsible for dysfunctional activity of tumor-specific CD8⁺T cells. These dynamic immunosuppressive networks prevent tumor rejection at several levels, limiting also the success of immunotherapies. Nevertheless, the recent clinical development of immune checkpoint inhibitors or of molecules modulating cellular targets and immunosuppressive enzymes highlights the great potential of approaches based on the selective disruption of immunosuppressive networks. Currently, the administration of different categories of immunotherapy in combination regimens is the ultimate modality for impacting the survival of cancer patients. With the advent of immune checkpoint inhibitors, designed to mount an effective antitumor immune response, profound changes occurred in cancer immunotherapy: from a global stimulation of the immune system to a specific targeting of an immune component. This review will specifically highlight the players, the mechanisms limiting an efficient antitumor response and the current immunotherapy modalities tailored to target immune suppressive pathways. We also discuss the ongoing challenges encountered by these strategies and provide suggestions for circumventing hurdles to new immunotherapeutic approaches, including the use of relevant biomarkers in the optimization of immunotherapy regimens and the identification of patients who can benefit from defined immune-based approaches.

100 项与 Veana Therapeutics, Inc. 相关的药物交易

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100 项与 Veana Therapeutics, Inc. 相关的转化医学

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当前项目

药物(靶点)	适应症	全球最高研发状态

VT-101(Veana Therapeutics)	HER2阳性乳腺癌更多	临床1期
Alpha-Tocopheryloxyacetic acid	淋巴瘤更多	临床1期
Vimo-005	实体瘤更多	无进展
Vimo-004	实体瘤更多	无进展
Vimo-V001	-	无进展