Top 5 Target	Count

NAMPT(Nicotinamide phosphoribosyltransferase)	13
FER(FER tyrosine kinase)	2
IKZF1 x IKZF3	2
Bcl-xl(Apoptosis regulator Bcl-X)	1
PARP1(Poly (ADP-Ribose) polymerase 1)	1

Drugs associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

GT-929

Target

IKZF1 x IKZF3

Mechanism

IKZF1 inhibitors [+1]

Active Org.

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Originator Org.

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Active Indication

Non-Hodgkin's lymphoma refractory [+4]

Inactive Indication-

Drug Highest PhasePhase 1/2

First Approval Ctry. / Loc.-

First Approval Date-

GT-919

Target

IKZF1 x IKZF3

Mechanism

IKZF1 inhibitors [+1]

Active Org.

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Originator Org.

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Active Indication

Multiple Myeloma [+1]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date-

GT818

Target-

Mechanism-

Active Org.

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Originator Org.

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Active Indication

Solid tumor

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date-

Clinical Trials associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

CTR20240122

/ RecruitingPhase 1

评估GT929在恶性血液肿瘤患者中的安全性、耐受性、药代动力学特征及初步疗效的I/IIa期临床研究

[Translation] Phase I/IIa clinical study to evaluate the safety, tolerability, pharmacokinetic characteristics and preliminary efficacy of GT929 in patients with malignant hematological tumors

单药剂量递增阶段：主要目的：评价GT929用于治疗复发或难治性非霍奇金淋巴瘤（rrNHL）或复发或难治性多发性骨髓瘤（rrMM）的安全性、耐受性；探索剂量限制性毒性（DLT），确定最大耐受剂量（MTD）或II期研究推荐剂量（RP2D）；次要目的：评价GT929在rrNHL或rrMM患者中的药代动力学（PK）特征；评价GT929在rrNHL或rrMM中的初步疗效。剂量扩展阶段：主要目的：评价GT929在rrNHL或rrMM中的有效性；次要目的：评价GT929在rrNHL或rrMM中的安全性。

[Translation]

Single-drug dose escalation phase: Primary purpose: To evaluate the safety and tolerability of GT929 for the treatment of relapsed or refractory non-Hodgkin lymphoma (rrNHL) or relapsed or refractory multiple myeloma (rrMM); To explore dose-limiting toxicity (DLT) and determine the maximum tolerated dose (MTD) or recommended dose (RP2D) for Phase II studies; Secondary purpose: To evaluate the pharmacokinetic (PK) characteristics of GT929 in patients with rrNHL or rrMM; To evaluate the preliminary efficacy of GT929 in rrNHL or rrMM. Dose expansion phase: Primary purpose: To evaluate the efficacy of GT929 in rrNHL or rrMM; Secondary purpose: To evaluate the safety of GT929 in rrNHL or rrMM.

Start Date27 Feb 2024

Sponsor / Collaborator

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

CTR20231255

/ RecruitingPhase 1

评估GT919在恶性血液肿瘤患者中的安全性、耐受性、药代动力学特征及初步疗效的I期临床研究

[Translation] A Phase I clinical study to evaluate the safety, tolerability, pharmacokinetic characteristics and preliminary efficacy of GT919 in patients with malignant hematological tumors

主要目的：评价GT919用于治疗复发或难治性多发性骨髓瘤（rrMM）或复发或难治性非霍奇金淋巴瘤（rrNHL）的安全性、耐受性；探索剂量限制性毒性（DLT），确定最大耐受剂量（MTD）；次要目的：评价GT919在rrMM或rrNHL患者中的药代动力学（PK）特征；评价GT919在rrMM或rrNHL中的疗效；确定II期研究推荐剂量（RP2D）。

[Translation]

Primary purpose: To evaluate the safety and tolerability of GT919 in the treatment of relapsed or refractory multiple myeloma (rrMM) or relapsed or refractory non-Hodgkin's lymphoma (rrNHL); to explore dose-limiting toxicity (DLT) and determine the maximum tolerated dose (MTD); Secondary purpose: To evaluate the pharmacokinetic (PK) characteristics of GT919 in patients with rrMM or rrNHL; to evaluate the efficacy of GT919 in rrMM or rrNHL; and to determine the recommended dose (RP2D) for Phase II studies.

Start Date03 Jul 2023

Sponsor / Collaborator

Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

100 Clinical Results associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

0 Patents (Medical) associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

Literatures (Medical) associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

02 Jan 2025·Cancer Research

Targeted Degradation of SOS1 Exhibits Potent Anticancer Activity and Overcomes Resistance in KRAS-Mutant Tumors and BCR–ABL–Positive Leukemia

Article

Author: Shen, Jie ; Wu, Wenyong ; Jiang, Hualiang ; Lin, Chencen ; Xie, Chengying ; Yuan, Changxian ; Wang, Sinan ; Luo, Ziwei ; Xu, Xiaowei ; Jiang, Biao ; Yu, Chuwei ; Yang, Xiaobao ; Wang, Yafang ; Sun, Renhong ; Wang, Dingyan ; Jia, Yan

AbstractSon of sevenless homolog 1 (SOS1) is an essential guanine nucleotide exchange factor for RAS that also plays a critical role in the activation of the small GTPase RAC mediated by BCR–ABL in leukemogenesis. Despite this, small-molecule inhibitors targeting SOS1 have shown limited efficacy in clinical trials for KRAS-mutant cancers, and their potential as a therapeutic approach for chronic myeloid leukemia (CML) remains largely unexplored. In this study, we developed a potent SOS1 proteolysis targeting chimera (PROTAC) SIAIS562055, which was designed by connecting a CRBN ligand to an analog of the SOS1 inhibitor BI-3406. SIAIS562055 exhibited sustained degradation of SOS1 and inhibition of downstream ERK pathways, resulting in superior antiproliferative activity compared with small-molecule inhibitors. SIAIS562055 also potentiated the activity of both KRAS inhibitors in KRAS-mutant cancers and ABL inhibitors in BCR–ABL–positive CML. In KRAS-mutant xenografts, SIAIS562055 displayed promising antitumor potency as a monotherapy and enhanced ERK inhibition and tumor regression when combined with KRAS inhibitors, overcoming acquired resistance. In CML cells, SIAIS562055 promoted the active uptake of BCR–ABL inhibitors by upregulating the carnitine/organic cation transporter SLC22A4. SIAIS562055 and BCR–ABL inhibitors synergistically enhanced inhibition of ABL phosphorylation and downstream signaling, demonstrating robust antitumor activities in both mouse xenografts and primary samples from patients with CML. In summary, this study suggests that PROTAC-mediated SOS1 degradation represents an effective therapeutic strategy for treating not only KRAS-mutant cancers but also BCR–ABL–harboring leukemia.Significance: The PROTAC SIAIS562055 sustainably degrades SOS1 and inhibits downstream ERK signaling, showing strong antiproliferative activity and synergistic effects with KRAS inhibitors in KRAS-mutant cancers and BCR–ABL inhibitors in chronic myeloid leukemia.

01 Dec 2024·Biochemical Pharmacology

Sorafenib and SIAIS361034, a novel PROTAC degrader of BCL-xL, display synergistic antitumor effects on hepatocellular carcinoma with minimal hepatotoxicity

Article

Author: Huang, Taomin ; Tan, Wenfu ; Zhang, Xiaoyi ; Tao, Yachuan ; Yang, Xiaobao ; Jiang, Biao ; Xu, Zhongli

The overexpression of BCL-x_L is closely associated with poor prognosis in hepatocellular carcinoma (HCC). While the strategy of combination of BCL-x_L and MCL-1 for treating solid tumors has been reported, it presents significant hepatotoxicity. SIAIS361034, a novel proteolysis targeting chimera (PROTAC) agent, selectively induces the ubiquitination and subsequent proteasomal degradation of BCL-x_L through the CRBN-E3 ubiquitin ligase. When combined with sorafenib, SIAIS361034 showed a potent synergistic effect in inhibiting hepatocellular carcinoma development both in vitro and in vivo. Since SIAIS361034 exhibits a high degree of selectivity for degrading BCL-x_L in hepatocellular carcinoma, the hepatotoxicity typically associated with the combined inhibition of BCL-x_L and MCL-1 is significantly reduced, thereby greatly enhancing safety. Mechanistically, BCL-x_L and MCL-1 sequester the BH3-only protein BIM on mitochondria at baseline. Treatment with SIAIS361034 and sorafenib destabilizes BIM/BCL-x_L and BIM/MCL1 association, resulting in the liberation of more BIM proteins to trigger apoptosis. Additionally, we discovered a novel compensatory regulation mechanism in hepatocellular carcinoma cells. BIM can rapidly respond to changes in the balance between BCL-x_L and MCL-1 through their co-transcription factor MEF2C to maintain apoptosis resistance. In summary, the combination therapy of SIAIS361034 and sorafenib represents an effective and safe approach for inhibiting hepatocellular carcinoma progression. The novel balancing mechanism may also provide insights for combination and precision therapies in the treatment of hepatocellular carcinoma.

01 Jun 2024·Cell Chemical Biology

NAMPT-targeting PROTAC and nicotinic acid co-administration elicit safe and robust anti-tumor efficacy in NAPRT-deficient pan-cancers

Article

Author: Yang, Xiaobao ; Jiang, Zhenzhou ; Liu, Haixia ; Zhang, Huijuan ; Zhu, Xiaotong ; Wang, Haopeng ; Fan, Gaofeng ; Xu, Bin ; Hou, Xianyu ; Wang, Yuetong ; Sun, Renhong ; Huang, Suming ; Jiang, Biao ; Li, Ye ; Hou, Chun

Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the biosynthesis of nicotinamide adenine dinucleotide (NAD⁺), making it a potential target for cancer therapy. Two challenges hinder its translation in the clinic: targeting the extracellular form of NAMPT (eNAMPT) remains insufficient, and side effects are observed in normal tissues. We previously utilized proteolysis-targeting chimera (PROTAC) to develop two compounds capable of simultaneously degrading iNAMPT and eNAMPT. Unfortunately, the pharmacokinetic properties were inadequate, and toxicities similar to those associated with traditional inhibitors arose. We have developed a next-generation PROTAC molecule 632005 to address these challenges, demonstrating exceptional target selectivity and bioavailability, improved in vivo exposure, extended half-life, and reduced clearance rate. When combined with nicotinic acid, 632005 exhibits safety and robust efficacy in treating NAPRT-deficient pan-cancers, including xenograft models with hematologic malignancy and prostate cancer and patient-derived xenograft (PDX) models with liver cancer. Our findings provide clinical references for patient selection and treatment strategies involving NAMPT-targeting PROTACs.

100 Deals associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

100 Translational Medicine associated with Biaoxin Biomedical Technology (Shanghai) Co., Ltd.

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Pipeline

Pipeline Snapshot as of 24 Jan 2025

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

Preclinical

Phase 1 Clinical

Phase 2 Clinical

Current Projects

Drug(Targets)	Indications	Global Highest Phase

GT-929 ( IKZF1 x IKZF3 )	Non-Hodgkin's lymphoma refractory More	Phase 2 Clinical
GT-919 ( IKZF1 x IKZF3 )	Multiple Myeloma More	Phase 1
GT818	Solid tumor More	Preclinical
SIAIS361034 ( Bcl-xl )	Neoplasms More	Preclinical
SIAIS630121 ( NAMPT )	Neoplasms More	Preclinical

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