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human immunoglobulin (pH4)

✓ Approved

Shenzhen Weiguang Biological · Polyclonal Antibodies · Polyclonal Antibodies

What is human immunoglobulin (pH4)?

human immunoglobulin (pH4) is a polyclonal antibodies developed by Shenzhen Weiguang Biological. It is approved for therapeutic indications via intraarterial injection or intravenous (iv).

Drug Profile

CompanyShenzhen Weiguang Biological
Drug ClassPolyclonal Antibodies, Antibody
RouteIntraarterial Injection, Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Shenzhen Weiguang Biological

Therapeutic Indications

human immunoglobulin (pH4) is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Immune system disordersImmunodeficiency✓ Approved

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PubMedCureus2026-09-20

Guillain-Barré Syndrome Revealing Coexisting Cervical Spondylotic Myelopathy: A Diagnostic Pitfall.

Boubekri Hatim H, Salah Anass A, Mankar Bennis Najoua N, Khalfaoui Saloua S et al.

Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy characterized by rapidly progressive weakness and areflexia. Although the diagnosis is usually straightforward, atypical clinical evolution should prompt investigation for concomitant central nervous system pathology. We report the case of a 64-year-old man initially diagnosed with severe GBS based on clinical presentation, cerebrospinal fluid (CSF) analysis, and electroneuromyography (EMNG) findings. Despite partial neurological improvement after intravenous immunoglobulin therapy, the patient later developed cervical pain, brisk reflexes, and a positive Babinski sign. Cervical magnetic resonance imaging (MRI) revealed severe multilevel cervical spondylotic myelopathy (CSM) with spinal cord compression and intramedullary T2 hyperintensity. Surgical decompression was subsequently indicated. This case highlights the importance of reassessing patients with GBS who develop pyramidal signs or atypical neurological findings, as concomitant cervical myelopathy may be overlooked and delay appropriate management.

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PubMedAsian Pacific journal of allergy and immunology2026-09-20

Type 2-interferon imbalance in allergic barrier disease: An asthma-centered, cross-disease perspective.

Rao Shenghong S, Li Shumei S, Shen Haoyue H, Jin Tengchuan T

Allergic diseases are typically regarded as type 2 inflammatory disorders driven by interleukin-4, interleukin-5, and interleukin-13, which mediate immunoglobulin E class switching, eosinophilic inflammation, mucus hypersecretion, pruritus, tissue remodeling, and epithelial barrier dysfunction. However, type 2 cytokine activity alone does not fully account for variations in exacerbation risk, susceptibility to infections, comorbidities, or responses to biologic therapy. This narrative review proposes an asthma-centered type 2-interferon imbalance framework and discusses its cautious, disease-specific extension to atopic dermatitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis, and food allergy. The model emphasizes that, particularly in asthma, allergic barrier inflammation arises and persists in injured tissues where excessive type 2 inflammation may coexist with impaired interferon-mediated host defense. Evidence is strongest in asthma, where deficiencies in type I and type III interferon responses are linked to rhinovirus susceptibility, delayed viral clearance, and recurrent exacerbations. In other allergic diseases, interferon dysfunction appears more variable, reflecting differences in tissue context, disease stage, and environmental exposure. In asthma, and potentially in selected allergic barrier diseases, persistent inflammation may result from a cycle of epithelial injury, alarmin release, cytokine amplification, impaired antiviral defense, ongoing exposure, and incomplete tissue repair. These mechanisms provide a rationale for tiered intervention, including blockade of upstream epithelial alarmins, inhibition of downstream type 2 effector pathways, and selected investigational approaches aimed at restoring mucosal host defense.

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PubMedCase reports in critical care2026-09-20

Pan-Neurofascin Antibody-Associated Nodopathy: A Critical Guillain-Barré Syndrome Mimic in the Differential Diagnosis-Report of Two Cases.

Nemethova Andrea A, De Ridder Willem W, Baar Ingrid I, Alonso-Jimenez Alicia A

Guillain-Barré syndrome (GBS) is an acute autoimmune polyradiculoneuropathy typically characterized by an ascending sensorimotor deficit with potential involvement of bulbar and respiratory muscles that may necessitate intensive care admission and mechanical ventilation. Standard treatment includes supportive care, management of complications such as weakness, immobility, respiratory failure, autonomic dysfunction and pain, along with early initiation of immunotherapy-either intravenous immunoglobulin (IVIg) or plasma exchange (PE). However, lack of significant clinical improvement following immunotherapy should prompt consideration of alternative diagnoses, including pan-neurofascin antibody-positive autoimmune nodopathy (panNF + AN). In this report, we present two patients presenting with a severe GBS-like neuropathy. Initial treatment with IVIg resulted in either no response or only transient, mild improvement, followed by rapid clinical deterioration to near-complete tetraplegia, respiratory failure, and autonomic and cranial nerve involvement. Both patients were unresponsive to further treatment with a second course of IVIg, PE and corticosteroids. Subsequent diagnostic evaluation revealed the presence of pan-neurofascin antibodies, confirming panNF + AN. This prompted initiation of treatment with rituximab, which resulted in sustained and complete clinical recovery in both cases. A transient or mild clinical response-or an initial lack of response-to standard GBS-treatment followed by rapid and severe deterioration in cases initially presenting as GBS should be considered a red flag warranting evaluation for AN-associated antibodies. Recognition of this important GBS mimic is critical, as it requires an alternative treatment approach with rituximab, which has been associated excellent clinical outcomes.

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Standards and Guidance for Transparent Disclosure of Human-Artificial Intelligence Collaboration Content in Medical Research (2026).

Medical Journals Committee of the Society of China University Journals

The rapid iteration of artificial intelligence (AI) tools is propelling medical research into a new phase characterized by human-AI collaboration.In the course of this process,AI has evolved from an external instrument into a functional component embedded within research workflows.As the collaborative boundary between human researchers and AI becomes increasingly ambiguous,governance challenges have grown increasingly salient.Concurrently,there remains a lack of internationally harmonized standards for the declaration of AI-assisted content,giving rise to notable disclosure gaps and implementation disconnects both domestically and abroad.To address these issues,the Professional Committee of Medical Journals of the Society of China University Journals assembled a multidisciplinary expert team covering fields such as medicine,biostatistics,epidemiology,medical ethics,scientific journal editing,and medical AI technology.Employing a modified Delphi method,the team conducted three rounds of online surveys and two consensus meetings.Drawing upon evidence from policy surveys of 1 692 medical journals,position statements from international organizations such as the International Committee of Medical Journal Editors,AI policy texts from the world's major academic publishers (Elsevier,Springer Nature,Wiley,Taylor & Francis,SAGE,etc.),and comparative studies on AI detection tool performance,the team ultimately formulated ten recommendations addressing core issues in medical publishing.This guidance emphasizes the core principles of transparent disclosure,human accountability,risk stratification,and technology-assisted oversight,aiming to fully harness the benefits of AI technology while upholding the bottom line of academic integrity.It provides a systematic framework for the standardized disclosure of human-AI collaboration content in medical research and offers actionable normative guidance for researchers,journal editors,peer reviewers,and academic institutions.

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PubMedOncogene2026-09-20

Beyond the blood-brain barrier: humanised mice, the missing link in glioblastoma research.

Shirazi Nia Reza R, Lu Jian J, De Vega Daniel D, Poudine Niloufar N et al.

Glioblastoma (GBM) remains a major challenge in neuro-oncology, associated with a high rate of mortality despite decades of intensive research and therapeutic advancements, underscoring the urgent need for innovative preclinical platforms that can more accurately recapitulate the biological and pathological features of human disease. While conventional animal models have contributed to our understanding of GBM biology and the evaluation of treatment efficacy, they fail to capture the full complexity and heterogeneity of the tumour microenvironment (TME). Ex vivo models are associated with certain advantages in this context; however, they can not mirror the complex dynamic and multicellular interactions present in living organisms, particularly the critical treatment barriers unique to the central nervous system: the blood-brain barrier (BBB), blood-cerebrospinal fluid barrier (BCSFB) and blood-meningeal barrier (BMB). In response to these limitations, humanised mouse models have emerged as an advanced platform capable of faithfully mimicking the molecular, pathological and immunological features of human GBM. These models enable the replication of complex in vivo crosstalk between the immune system and the TME, while preserving the relevant treatment barriers that govern drug delivery to the brain. Accumulating evidence indicates that humanised mouse models closely reproduce the infiltration of human immune components into the TME, enabling the study of clinically relevant interactions that contribute to therapeutic resistance and treatment failure in GBM. This review aims to provide a comprehensive and systematic overview of the currently employed humanised mouse models in GBM research, highlighting their applications and comparative advantages. Finally, we evaluate the opportunities and challenges associated with each model and discuss future directions to increase the translational relevance and predictive power of preclinical GBM research. Humanised mouse models provide a valuable translational platform combining the human immune system and PDX orthotopic engraftment. Compared to conventional models and ex vivo models, these models can reproduce the complex cross-talk between tumour cells and the immune system, tumour heterogeneity, immunosuppressive TME, as well as complex in vivo interactions such as brain-specific barriers, including BBB, BCSFB and BMB. Future implementation of the human gut microbiome in these models has the potential to further increase translational relevance and precision in GBM research. Created in BioRender.com.

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PubMedComprehensive physiology2026-09-20

Axial Connectivity of the Lung Microbiome: A Review of Interorgan Crosstalk.

Palanivel Mathangi M, Narayana Jayanth Kumar JK, Chotirmall Sanjay H SH

The classic organ-centric model of human physiology is rapidly giving way to a unified approach embracing the human body as an integrated network of bidirectional interorgan communication. The human microbiome serves as a fundamental mediator of this shift, regulating immune homeostasis, barrier integrity and metabolic signaling across organs. While the lung maintains a characteristic low-biomass microbiome in dynamic equilibrium, any disruption primes local and systemic immune responses contributing to disease. Beyond the well-described gut-lung axis, crosstalk between the lung and other distal organ systems is lesser recognized; however, increasingly acknowledged as a key under-appreciated contributor to respiratory disease including extrapulmonary complications. This review synthesizes current established evidence on axial connectivity of the lung microbiome across the gut, brain, skin, heart, kidney, and liver, and finds that such crosstalk is predominantly, though not exclusively gut-mediated. Direct lung-organ interactions are described for several axes; however, they remain preliminary. Across these lung-axial systems, common pathophysiological mechanisms emerge, including dysbiosis-induced depletion of microbial metabolites, immunomodulation, and barrier perturbations, all linking pulmonary disease with neuroinflammation, gastrointestinal deficits, and cardiac, renal, hepatic, and dermatological abnormalities. We assess how therapeutic modulation of interorgan systems offers promising avenues for improved risk stratification and novel therapeutics. Recognizing microbiome-mediated pulmonary-organ crosstalk represents an emerging conceptual framework in respiratory medicine, repositioning microbial communities as key modulators of extrapulmonary disease.

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