This issue selects 8 cutting-edge pharmaceutical achievements: Shanghai Jiao Tong University team discovered new biomarkers for precise identification of Parkinson’s disease and multiple system atrophy; Six Asian countries release their first roadmap for synthetic cell technology; C5a monoclonal antibody STSA-1002 provides new clues for the treatment of ARDS; Tongji University reveals brown fat releasing energy vesicles for repairing damaged hearts; Sun Yat sen University proposes the combination of immunotherapy and local chemotherapy to overcome the dilemma of advanced liver cancer; The Chinese Academy of Sciences has discovered a new mechanism by which fructose inhibits liver cancer by “attacking poison with poison”; The team of the University of Science and Technology of China revealed the “stealth” and treatment targets of pancreatic cancer; Shanghai Institute of Hematology elucidates the mechanism of IGF2BP2 promoting PTCL immune escape. Multiple studies have provided new targets and strategies for neurodegenerative diseases, cardiovascular diseases, tumors, and more.

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1、 Shanghai Jiao Tong University team’s latest research achieves precise identification of Parkinson’s disease and multiple system atrophy

The team led by Li Dan from Shanghai Jiao Tong University published a research paper online in Cell on the evening of the 26th Beijing time, discovering and verifying a new biomarker for synucleinopathy – microtubule polymerization promoting protein (TPPP/p25). They found the “typing code” in cerebrospinal fluid, achieving precise identification between Parkinson’s disease and multiple system atrophy.

Parkinson’s disease and multiple system atrophy are two neurodegenerative diseases that look very similar but are fundamentally different. Patients may experience symptoms such as bradykinesia, tremors, and unstable walking in the early stages, which are difficult to accurately distinguish based solely on clinical examination. However, incorrect diagnosis may mean missing the optimal intervention timing and even leading to the wrong treatment direction.

Based on structural information, the team designed a protein fragment called miniCORE. This’ super bait ‘is like a highly sensitive detector and amplifier, capable of accurately identifying trace amounts of TPPP/p25 pathological seeds and amplifying the signal to a detectable level. Thus, the team established a TPPP/p25-SAA detection method.

The research team spent seven years overcoming difficulties step by step. In the testing of over 200 clinical samples, the results of the new method were exciting: cerebrospinal fluid samples from patients with multiple system atrophy triggered strong amplification reactions, while samples from other diseases such as Parkinson’s disease, Alzheimer’s disease, and Lewy body dementia did not show significant responses. This means that this new ‘bait’ can indeed ‘catch accurately and distinguish clearly’. It is reported that the value of this achievement lies not only in a scientific discovery, but also in its direct targeting of clinical pain points. Patients can obtain cerebrospinal fluid through lumbar puncture, which is expected to provide a clear diagnosis in the early stages of the disease, no longer being uncertain about whether it is like Parkinson’s or multiple system atrophy, and thus seize an earlier treatment window. At present, the TPPP/p25-SAA detection method is mainly based on cerebrospinal fluid samples, and the research team is also exploring the possibility of extending it to other body fluids such as blood to reduce the invasiveness of the detection.

2、 Scholars from six Asian countries propose the first roadmap for synthetic cell technology in Asia

On May 26, led by researcher Liu Chenli of the Chinese Academy of Sciences Shenzhen Institute of Advanced Technology, the “Asian Synthetic Cell Alliance”, composed of more than 100 laboratories in six Asian countries, published an article in the world’s top journal Nature Biotechnology, officially releasing the world’s first regional level synthetic cell technology roadmap, outlining the research and development path in the field of the next decade, marking that Asian synthetic cell research has officially entered a new stage of collaboration from decentralized exploration.

Synthetic cells are the core direction of synthetic biology, and also the core underlying technology platform for the next generation of biomedicine and green biomanufacturing. In recent years, the global field has rapidly advanced, but the systemic bottleneck of designing and constructing complex life systems has not been overcome. Countries’ dispersed research and development lack top-level collaboration, and key breakthroughs have yet to be achieved. As the fastest-growing region in synthetic biology globally, Asia has its own advantages in niche areas such as DNA synthesis, chassis modification, and quantitative biology. However, the long-term lack of a unified collaborative mechanism and resource mismatch have delayed the breakthrough process in these fields.

This roadmap systematically outlines the four core challenges faced in the construction of synthetic cells, innovatively proposes a new research paradigm that combines rational “white box” design with directed evolution “black box” optimization, pioneers an open cross-border resource sharing and collaboration model, and clearly sets two-stage research and development goals: the first stage is to overcome core technological bottlenecks and build “primitive cells” that can be autonomously replicated; The second stage is to gradually upgrade the technological system and move towards customized “autonomous cells”.

The six Asian countries have proposed a “central factory+distributed workstations” model to solve the problem of synthesizing cells. Image provided by the interviewed unit

This roadmap is a representative original achievement of collaborative innovation in cutting-edge life sciences in Asia, which will promote the transformation of global synthetic cell research from decentralized trial and error to systematic collaborative construction, and clear the path obstacles for the industrialization of synthetic cells in the fields of innovative drug development, engineered cell therapy, and other biomedical fields.

3、 C5a monoclonal antibody STSA-1002 provides new clues for the treatment of ARDS

Acute respiratory distress syndrome (ARDS) is the leading cause of death in patients with severe viral pneumonia. Currently, only symptomatic interventions such as respiratory support can be provided in clinical practice, and there is a lack of specific therapeutic drugs that can improve long-term prognosis. The clinical needs in this field are extremely urgent. In recent years, basic research has shown that excessive activation of the complement system is the core mechanism driving viral pneumonia inflammation storm and exacerbating lung injury. C5a, as the core pro-inflammatory mediator of the complement cascade reaction, is a potential target for ARDS treatment, and targeting the C5a pathway is highly anticipated by the academic community.

Led by Cao Bin and Wang Yeming from the China-Japan Friendship Hospital and participated by several centers in China, the Phase 1b/2 study of C5a monoclonal antibody STSA-1002 announced that the study included 18-85 years old patients with viral pneumonia related ARDS, and explored the efficacy and safety of different doses through randomized stratified design. The preclinical study has verified that STSA-1002 can reduce the death risk of severe pneumonia related ARDS. The results of this clinical study show that the median time for clinical improvement of patients in the 1350mg dose group is significantly shorter, the 28 day all-cause mortality rate shows a clear downward trend, and the overall drug tolerance is good, without unexpected serious adverse events.

As an exploratory study, due to sample size limitations, the conclusions of this study still need to be validated by three confirmatory studies. At present, the team has clarified that the subsequent Phase 3 studies will use 1350mg as the core trial dose, with 28 day all-cause mortality as the primary endpoint, and simultaneously explore the advantageous population for benefits. This study provides the first clinical evidence of C5a inhibition strategy for the treatment of ARDS in the Chinese population, laying a solid foundation for subsequent confirmatory research. If phase 3 validation is successful, it will fill the gap in targeted therapy in the field of ARDS.

4、 Nat Communi: Brown fat releases energy vesicles to repair damaged heart

The global burden of cardiovascular disease continues to rise, and pathological myocardial remodeling after myocardial infarction is the core pathological link that progresses to heart failure and leads to patient death. Currently, there is still a lack of specific intervention methods to effectively block remodeling in clinical practice. On May 21, 2026, the team led by Xiang Yaozu from Tongji University published their latest research in the international journal Nature Communications, which for the first time elucidated the cross organ communication mechanism of brown adipose tissue (BAT) regulating cardiac remodeling, providing a new intervention target and drug development direction for this disease field.

Previous studies have only confirmed the systemic protective effect of BAT on cardiovascular injury, but the functional communication mediators and regulatory mechanisms between BAT and the distal heart have long been inconclusive. This study clarified through in vivo tracing, molecular functional validation, and quantitative proteomic analysis that under myocardial ischemic stress, BAT can translocate to mitochondria through VPS35, drive functional mitochondrial protein sorting and assembly, form mitochondrial derived vesicles (MDVs), and secrete them into the circulation loop; The sorting secretion process strictly relies on Becn1 regulation, and the absence of Becn1 completely blocks MDV generation, eliminating the cardioprotective effect of BAT.

Research has confirmed that circulating MDVs can target and migrate to damaged hearts, where they are taken up by resident macrophages and exert significant anti-inflammatory effects, thereby reducing pathological remodeling; Proteomics further identified mitochondrial respiratory chain complex V as a core marker component of protective MDVs. Animal experiments showed that administration of purified complex V enriched MDVs significantly improved cardiac remodeling damage in myocardial infarction model mice. This study reveals a novel mechanism of cross organ bioenergy unit transport, opening up a new path for the development of innovative extracellular vesicle drugs for post myocardial infarction remodeling.

5、 Immune combined local chemotherapy regimen breaks through the treatment dilemma of advanced liver cancer

The combination of advanced hepatocellular carcinoma (HCC) and portal vein thrombosis (PVTT) is currently a core challenge in the clinical diagnosis and treatment of liver cancer. Patients with Vp3/Vp4 grade PVTT (tumor thrombus involving the main or branching portal vein) have extremely poor prognosis, limited benefits from existing standard treatment regimens, and a median overall survival (OS) of less than 10 months, indicating an urgent unmet clinical need. Recently, the team led by Lv Ning and Zhao Ming from the Cancer Prevention and Treatment Center of Sun Yat sen University published the results of their Phase II clinical research in Nature Communications, providing a potential new treatment plan for this difficult to treat population.

The DurHope single arm phase II clinical trial conducted by the team included a total of 30 advanced HCC patients with Vp3/Vp4 grade PVTT. The combination regimen of PD-L1 inhibitor durvalumab and FOLFOX hepatic artery infusion chemotherapy was used: this design not only achieved rapid tumor shrinkage and induced tumor antigen release through local high concentration chemotherapy, but also cooperated with immune checkpoint inhibitors to relieve tumor immune suppression and exert synergistic anti-tumor effects. The research results showed that the 1-year OS rate of patients treated with this combination therapy reached 63.3%, with a median OS of 13.9 months. The efficacy was significantly better than the historical data of traditional regimens, and the overall adverse reactions were controllable, with no unexpected serious adverse events.

Further molecular stratification analysis showed that non responsive patients were significantly enriched in molecular features related to chemotherapy resistance and immune escape, while responders had significantly higher levels of anti-tumor immune infiltration in their tumor tissues. The research team has identified potential efficacy predictive biomarkers, providing molecular evidence for subsequent precise stratified treatment. This study provides a new treatment direction for advanced HCC with high-grade PVTT and lays the foundation for subsequent phase III confirmatory trials.

6. IF=53！ Fructose ‘uses poison to attack poison’ to inhibit liver cancer, while ebselenidine may become a new anti-cancer weapon

Primary liver cancer is a highly prevalent malignant tumor in China, and the objective response rate of systemic treatment for advanced liver cancer is still less than 30%. There is an urgent need for the development of new targets and therapies. Recently, the team of Yin Huiyong from the Chinese Academy of Sciences Shanghai Institute of Nutrition and Health made breakthrough progress in the field of tumor metabolism, first identified the core mechanism of fructose metabolism intervention to kill liver cancer cells, and verified the anticancer activity of the clinical drug ibuselene, opening up a new path for precise treatment of liver cancer.

This study revealed a unique metabolic weakness of liver cancer cells: liver cancer cells generally downregulate the expression of the key enzyme aldolase B (ALDOB) in fructose metabolism, which can promote glucose metabolism reprogramming and support rapid proliferation of cancer cells. However, this change also brings metabolic defects – when fructose enters liver cancer cells lacking ALDOB, the generated fructose-1-phosphate (F1P) cannot be metabolized normally, and a large amount of accumulated F1P competitively inhibits the activity of mannose-6-phosphate isomerase (MPI), disrupts the endoplasmic reticulum glucose homeostasis of cells, triggers unfolded protein response, and ultimately induces endoplasmic reticulum stress-induced apoptosis of liver cancer cells, achieving the special effect of fructose “targeted anti-cancer”.

Further research has confirmed that the clinically applied ebselenidin is a highly active MPI inhibitor that can mimic the anticancer effect of F1P, and only exerts a killing effect on liver cancer with low expression of ALDOB. In the future, clinical trials can stratify the benefit population by detecting the expression of ALDOB in patients, and promote the precise treatment application of ebselenidin. This study is based on the development of a new approach using old drugs, which combines mechanism originality and translational feasibility, providing a new strategy for the rapid implementation of liver cancer treatment.

7、 Chinese University of Science and Technology team reveals “stealth” and therapeutic potential of pancreatic cancer

As a malignant tumor of digestive system with poor prognosis, pancreatic cancer has a 5-year survival rate of less than 10%. The overall response rate of existing immunotherapy is extremely low. The immune stealth mechanism of tumor cells is a core scientific problem in the field that needs to be solved urgently. Recently, Liu Lianxin’s team from the University of Science and Technology of China published the latest research results in the international authoritative journal Advanced Science, which systematically clarified the new molecular mechanism of pancreatic cancer to escape immune killing, providing a clear new target direction for clinical treatment of pancreatic cancer.

This study confirmed for the first time through a large sample of clinical omics analysis that the palmitoyl transferase ABHD17C was abnormally high expressed in pancreatic cancer tissue, and its expression level was significantly related to the poor prognosis of patients. Studies at the mechanism level have confirmed that ABHD17C can specifically catalyze the depomylation of cysteine 442 of the tumor suppressor protein BCL6B (B-cell lymphoma 6 family protein B). This modification, on the one hand, prevents BCL6B nuclear translocation to achieve transcriptional regulation function, on the other hand, promotes BCL6B ubiquitination degradation, and ultimately weakens the transcriptional inhibition of BCL6B on the downstream target gene CD24, resulting in abnormal overexpression of CD24 in pancreatic cancer cell membrane.

As a classic “don’t eat me” immune signal, CD24 overexpression can help pancreatic cancer cells escape from phagocytosis and killing of macrophages, and achieve immune invisibility. This study clarified the complete function of ABHD17C/BCL6B/CD24 signal axis to promote immune escape, confirmed that targeting this pathway to regulate innate immunity has a clear clinical therapeutic potential for pancreatic cancer, and provided a clear molecular blueprint for subsequent targeted drug development.

8、 Shanghai Institute of Hematology discovers IGF2BP2 promotes PTCL immune escape mechanism

Peripheral T-cell lymphoma (PTCL) is a highly heterogeneous and invasive malignant tumor of the lymphatic hematopoietic system originating from mature T cells. The overall prognosis is poor, and the response rate of existing first-line treatment options is less than 50%. There is a long-term lack of precise therapeutic targets based on pathogenic mechanisms, and functional markers and therapeutic potential at the RNA epigenetic modification level have not been fully explored. On May 21, 2026, the team led by Zhao Weili and Xiong Jie from the Shanghai Institute of Hematology published a groundbreaking study in the top international hematology journal Blood, systematically elucidating the core mechanism of IGF2BP2 driven immune escape in PTCL by the m ⁶ A reader, opening up new directions for precision treatment of PTCL.

This study found through multi omics analysis of clinical PTCL samples that the m ⁶ A modified reader IGF2BP2 was significantly upregulated in PTCL tumor cells and significantly correlated with poor prognosis in patients. At the mechanistic level, IGF2BP2 can upregulate target protein expression by recognizing the m ⁶ A modification site of endocytic regulatory gene mRNA, enhance mRNA stability, and thereby enhance tumor cell endocytosis activity. It promotes the internalization and degradation of the cell surface antigen presenting core molecule MHC and immune activation related receptor KLRC1/DIPOR1, ultimately promoting malignant proliferation of PTCL tumor cells and inhibiting the activation and infiltration of CD8 ⁺ effector T cells in the tumor microenvironment, mediating tumor immune escape.

Functional validation shows that the IGF2BP2 targeted inhibitor CWI1-2 can significantly inhibit PTCL growth in vitro and in vivo models, while reshaping the tumor immune microenvironment and restoring anti-tumor immune response. PTCL with high IGF2BP2 expression is more sensitive to this inhibitor. This study established the oncogenic driving role of IGF2BP2 in PTCL and established a direct mechanism association between m ⁶ A modification and PTCL immune escape, providing a key theoretical basis for RNA modified PTCL treatment strategies.

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