Generium Pharmaceutical · Recombinant Proteins · Recombinant Proteins
interferon beta-1b is a recombinant proteins developed by Generium Pharmaceutical. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.
| Brand Names | Infibeta |
| Company | Generium Pharmaceutical |
| Drug Class | Recombinant Proteins |
| Route | Injectable (Others), Subcutaneous Injection |
| Status | Approved |
interferon beta-1b is developed for 1 unique indication across 1 therapeutic area.
| Therapeutic Area | Condition | Phase |
|---|---|---|
| Nervous system disorders | Multiple sclerosis | ✓ Approved |
Zhygalova Zhygalova Ilona I, Blanco López Iago I, Dopazo Sotillo Silvia S, Carreira Sampayo Uxía U et al.
Borutzki Yasmin Y, Hagn Gerhard G, Bileck Andrea A, Mohr Thomas T et al.
BOLD-100 (sodium trans-[tetrachlorobis(1H-indazole)ruthenate(III)]) is a clinical-stage anticancer drug candidate that targets glucose-regulated protein (GRP78) and impacts the endoplasmic reticulum (ER) stress responses in cancer cells. Despite expanding knowledge about its multimodal mechanism of action from preclinical studies, little is known about the metabolic effects of BOLD-100 in patients. This study is an exploratory analysis of the blood plasma from a subset of metastatic colorectal carcinoma (mCRC) patients who were participants in a phase 1b/2a dose-escalation study (NCT04421820) using a multi-omics strategy based on proteomic and lipid analyses. BOLD-100 treatment was found to exhibit systemic, dose-dependent effects that were more pronounced on the lipid level compared with the protein level. This study indicates that BOLD-100 affects lipid profiles and influences systemic lipid crosstalk, which, in combination with oxaliplatin, leucovorin, and fluorouracil (FOLFOX) chemotherapy may, at least partially, account for the superior clinical outcomes over established therapies in mCRC patients.
Morgan Rachel K RK, Matei Evelyn K EK, Pan Junru J, Ishikawa Tomoko T et al.
Developmental neurotoxicant exposures (e.g., lead [Pb]) are suspected contributors to dementia. Dementia is characterized by amyloid beta (Aβ) plaques and dysregulated metabolism. To better understand the relationship between environment and dementia risk, we assessed the impact of perinatal Pb exposure on dementia-related outcomes in the murine brain. Female mice were exposed to 32 ppm Pb or control water during gestation and lactation. Offspring were aged out to 3 weeks or 18 months. We measured Aβ in the 18-month cortex and performed untargeted metabolomics in plasma and cortex at 3 weeks and 18 months of age. Diffuse Aβ and Aβ-positive cells were significantly elevated with Pb exposure. Pb-associated metabolites were enriched for those implicated in oxidative stress, inflammation, and lipid metabolism. Pb was associated with molecular and metabolic features of dementia. Important biochemical classes provide insights into possible mechanisms by which developmental Pb exposure may contribute to dementia risk.
Ureshino Hiroshi H
The introduction of tyrosine kinase inhibitors (TKIs) has made long-term survival achievable for patients with chronic myeloid leukemia (CML). In patients who achieve a deep molecular response, treatment-free remission (TFR), defined as sustained remission without molecular relapse after TKI discontinuation, has emerged as an important therapeutic goal. Accumulating evidence indicates that the establishment and maintenance of TFR are strongly influenced by host immunity, particularly immune surveillance mediated by natural killer (NK) cells. This review summarizes the clinical and immunological factors associated with successful TFR and discusses the potential of killer immunoglobulin-like receptor/human leukocyte antigen genetic polymorphisms as predictive biomarkers that regulate NK cell function and TFR outcomes. It also highlights immunomodulatory strategies using interferon-α, the feasibility of second attempts at TFR after initial discontinuation failure, and emerging therapeutic approaches targeting CML stem cells to achieve more durable disease control.
Ogor Thomas Teja TT, Porée Esther E, Saenz Javier J, Davieau Marion M et al.
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host immune response, characterized by both hyperinflammation and immunosuppression. Here, we show that the absence of the C-type lectin receptor CLEC-1-expressed particularly by lung cDC1s-improves mouse recovery following E. coli infection. Mechanistically, phenotypic and transcriptomic analyses revealed that Clec1a loss is characterized by an attenuated type I interferon response in lung cDC1s as well as reduced CXCL10 expression and monocyte infiltration during the acute phase of sepsis. Additionally, Clec1a deficiency is associated with an enhanced antigen presentation profile of lung myeloid cells and lower accumulation of regulatory T cells upon secondary infection, suggesting reduced immunoparalysis. Importantly, we demonstrate that blocking CLEC-1 using an anti-human CLEC-1 monoclonal antibody mitigates hyperinflammation in CLEC-1 humanized mice. Together, these findings uncover a role for CLEC-1 in the dysregulation of the inflammatory response during sepsis and suggest its potential as an immunotherapeutic target.
Wang Ren-Yi RY, Danciu Diana-Patricia DP, Klawe Filip Z FZ, Marciniak-Czochra Anna A
Inter-individual heterogeneity is often treated as noise, yet its temporal evolution can reveal regulatory mechanisms hidden from mean-field behavior. We present a stochastic framework that exploits variability for mechanistic inference in cell population dynamics. Using adult neurogenesis as a case study, we develop a state-dependent stochastic model of transitions between quiescent and active states and derive a diffusion approximation for the dynamics of both mean and variance. Applied to repeated cross-sectional data from wild-type and interferon-receptor knockout mice, we show that distinct regulatory mechanisms can produce similar mean dynamics but different fluctuation patterns. Jointly fitting mean and variance identifies proliferation-rate regulation as the dominant contributor to variability, while activation and self-renewal primarily govern average and long-term dynamics. Wild-type mice exhibit regulation of all three processes, whereas knockout mice lose activation control. These results show that population-level variability provides mechanistic information beyond average dynamics and helps distinguish between competing mechanistic models.
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