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更新于：2025-10-11
TY-101
更新于：2025-10-11
概要
基本信息
原研机构 |
在研机构 |
非在研机构- |
权益机构- |
最高研发阶段临床1/2期 |
首次获批日期- |
最高研发阶段(中国)临床1/2期 |
特殊审评- |
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结构/序列
Sequence Code 2545CDR2-L
Sequence Code 4404CDR1-H
Sequence Code 13417166CDR3-L
Sequence Code 407340749CDR2-H
Sequence Code 407340751CDR3-H
Sequence Code 407340753CDR1-L
Sequence Code 407340795VH
Sequence Code 432498916VL
关联
1
项与 TY-101 相关的临床试验NCT04458389
Phase 1 (Dose Escalation)/Phase 2 (Expansion Cohort) Trial of TY101 as a Single Agent in Patients With Locally Advanced/Metastatic Solid Tumors and Relapsed or Refractory Lymphomas
100 项与 TY-101 相关的临床结果
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100 项与 TY-101 相关的转化医学
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100 项与 TY-101 相关的专利（医药）
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3
项与 TY-101 相关的文献（医药）2023-02-01Cellular oncology (Dordrecht)
TNFR2 antagonistic antibody induces the death of tumor infiltrating CD4+Foxp3+ regulatory T cells
Article
作者: Faustman, Denise L ; Oppenheim, Joost J ; He, Tianzhen ; Chou, Chon-Kit ; Chen, Xin ; Yang, De ; Chen, Yibo ; Liu, Jiarui ; Islam, Md Sahidul
BACKGROUND:
TNFR2 expression is a characteristic of highly potent immunosuppressive tumor infiltrating CD4+Foxp3+ regulatory T cells (Tregs). There is compelling evidence that TNF through TNFR2 preferentially stimulates the activation and expansion of Tregs. We and others, therefore, proposed that targeting TNFR2 may provide a novel strategy in cancer immunotherapy. Several studies have shown the effect of TNFR2 antagonistic antibodies in different tumor models. However, the exact action of the TNFR2 antibody on Tregs remained understood.
METHOD:
TY101, an anti-murine TNFR2 antibody, was used to examine the effect of TNFR2 blockade on Treg proliferation and viability in vitro. The role of TNFR2 on Treg viability was further validated by TNFR2 knockout mice and in the TY101 antagonistic antibody-treated mouse tumor model.
RESULTS:
In this study, we found that an anti-mouse TNFR2 antibody TY101 could inhibit TNF-induced proliferative expansion of Tregs, indicative of an antagonistic property. To examine the effect of TY101 antagonistic antibody on Treg viability, we treated unfractionated lymph node (L.N.) cells with Dexamethasone (Dex) which was known to induce T cell death. The result showed that TY101 antagonistic antibody treatment further promoted Treg death in the presence of Dex. This led us to find that TNFR2 expression was crucial for the survival of Tregs. In the mouse EG7 lymphoma model, treatment with TY101 antagonistic antibody potently inhibited tumor growth, resulting in complete regression of the tumor in 60% of mice. The treatment with TY101 antagonistic antibody elicited potent antitumor immune responses in this model, accompanied by enhanced death of Tregs.
CONCLUSION:
This study, therefore, provides clear experimental evidence that TNFR2 antagonistic antibody, TY101, can promote the death of Tregs, and this effect may be attributable to the antitumor effect of TNFR2 antagonistic antibody.
2021-12-01International immunopharmacology2区 · 医学
A TNFR2 antibody by countering immunosuppression cooperates with HMGN1 and R848 immune stimulants to inhibit murine colon cancer
2区 · 医学
Article
作者: Li, Ping ; Oppenheim, Joost J ; Faustman, Denise L ; Jiang, Mengmeng ; Chen, Xin ; Chen, Fengyang ; Yang, De ; Alam, Md Masud ; Tross, Debra ; Liu, Jia
Immunosuppressive CD4+Foxp3+ regulatory T cells (Tregs) promote tumor immune evasion and thus targeting of Tregs has become an strategy in cancer immunotherapy. Tumor necrosis factor receptor 2 (TNFR2) is highly expressed and important for the immunosuppressive function of Tregs in humans and mice. Thus, the benefit of targeting TNFR2 in cancer immunotherapy merits more investigation. A previous report identified a new murine monoclonal anti-TNFR2 antibody (designated TY101), which showed therapeutic efficacy in murine cancer models, but its mechanism of action was less understood. In this study, the capacity of a combination of immunostimulants to enhance the effect of this inhibitor of Tregs was investigated. We examined the efficacy of TY101 as an anti-tumor immune reagent combined with HMGN1 (N1, a dendritic cell activating TLR4 agonist) and R848 (a synthetic TLR7/8 agonist). This immunotherapeutic combination exerted synergistic antitumor effects as compared with any single treatment. The antitumor response was mainly mediated by the depletion of Tregs and stimulation of cytotoxic CD8 T cell activation. The result also suggested that the effect of TY101 was similar to that of anti-PD-L1 when used in combination with these immunostimulants. Therefore, we propose that treatment strategies of antagonizing TNFR2 on Tregs would behave as potent checkpoint inhibitors and can potentially be utilized to develop a novel antitumor immunotherapy.
2016-01-01International journal of medical sciences3区 · 医学
Association of Far-Infrared Radiation Therapy and Ankle-Brachial Index of Patients on Hemodialysis with Peripheral Artery Occlusive Disease
3区 · 医学
ArticleOA
作者: Hwang, Shang-Jyh ; Mai, Hsiu-Chin ; Huang, Jiun-Chi ; Kuo, Po-Lin ; Chang, Jer-Ming ; Lee, Mei-Yueh ; Kuo, I-Ching ; Chen, Szu-Chia ; Chen, Hung-Chun
Background and Aim: The ankle-brachial index (ABI) is recognized to be a good marker for atherosclerosis, and is useful in the diagnosis of peripheral artery occlusive disease (PAOD) which is prevalent among patients on hemodialysis (HD). Methods: This randomized trial aimed to evaluate the effect of far-infrared radiation (FIR) therapy on ABI in HD patients with PAOD. PAOD was defined as patients with ABI < 0.95. One hundred and eight HD patients were enrolled, including 50 in the control group and 58 in the FIR group. A WS TY101 FIR emitter was applied for 40 minutes during each HD session, three times per week for six months. The ABI was measured before and after the FIR therapy. Results: Regardless of FIR therapy, the bilateral ABI decreased (in the FIR group, left: 0.88±0.22 to 0.85±0.24, p = 0.188; right: 0.92±0.20 to 0.90±0.23, p = 0.372; in control group, left: 0.91±0.23 to 0.88±0.21, p = 0144; right: 0.93±0.17 to 0.89±0.21, p = 0.082). Multivariate logistic analysis of the FIR group revealed that high uric acid (odds ratio [OR]: 2.335; 95% confidence interval [CI]: 1.117-4.882; p=0.024) and aspirin use (OR: 16.463; 95% CI: 1.787-151.638; p=0.013) were independently associated with increased bilateral ABI after FIR therapy. Conclusions: This study demonstrates that ABI is not increased after FIR therapy in HD patients with PAOD. However, in the FIR group, patients with higher uric acid level or those who used aspirin have increased bilateral ABI after FIR therapy.
1
项与 TY-101 相关的新闻（医药）2025-09-29
·靶点圈
免疫疗法临床终止ASH会议临床结果
100 项与 TY-101 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 晚期淋巴瘤 | 临床2期 | 中国 | 2020-12-07 | |
| 晚期恶性实体瘤 | 临床2期 | 中国 | 2020-12-07 | |
| 局部晚期恶性实体瘤 | 临床2期 | 中国 | 2020-12-07 | |
| 难治性T细胞淋巴瘤 | 临床2期 | 中国 | 2020-12-07 |
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