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interferon alfa-2a (Proquiferon)

✓ Approved

Probiomed · IFNAR2 · Recombinant Proteins

What is interferon alfa-2a?

interferon alfa-2a is a recombinant proteins developed by Probiomed. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection or subcutaneous injection.

Drug Profile

Brand NamesProquiferon
CompanyProbiomed
Drug ClassRecombinant Proteins
Molecular TargetIFNAR2
RouteInjectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Probiomed

Mechanism of Action

Molecular Targets

interferon alfa-2a acts on 1 molecular target:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
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Therapeutic Indications

interferon alfa-2a is developed for 8 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsAcquired immunodeficiency syndrome✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Kaposi's sarcoma✓ Approved

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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.

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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.

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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.

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Wang Ren-Yi RY, Danciu Diana-Patricia DP, Klawe Filip Z FZ, Marciniak-Czochra Anna A

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Pre-emptive genotyping and genotype-guided dose adjustments are generally recommended for seven hypofunctional polymorphisms in the DPYD gene that are associated with fluoropyrimidine toxicity. However, targeted genotyping may miss uncommon and population-specific hypofunctional variants. Therefore, in 2021, we replaced conventional targeted genotyping with comprehensive DPYD exome sequencing. The objective of the current study was to identify uncommon hypofunctional variants and assess their association with fluoropyrimidine toxicity. In a cohort of 762 consecutive patients pre-emptively genotyped between 2021 and 2025, among the seven established risk variants, we identified *2A and HapB3 at their expected minor allele frequencies (MAF), but no carriers of any of the five other established risk variants. Interestingly, four patients were heterozygous for the rare missense c.257C>T variant (Pro86Leu; rs568132506), previously associated with fluoropyrimidine toxicity. The MAF (2.62 × 10-3) was similar to that previously described in Middle Eastern populations but 26-fold higher than in the gnomAD global population. Three of the carriers (75%) developed grade 3-4 fluoropyrimidine toxicity after one or two cycles, corresponding to a relative risk of 14.5 (95% confidence interval: 5.0-30.4, P = 0.0009) compared with a control cohort without hypofunctional DPYD variants. Our findings add to the growing body of evidence indicating that DPYD c.257C>T may be associated with severe fluoropyrimidine toxicity. Future studies should examine the clinical utility of including uncommon but potentially actionable variants, such as c.257C>T, into pre-emptive genotyping algorithms. This may be particularly important in multiethnic populations in which these variants can be more prevalent than those variants for which pre-emptive genotyping is generally recommended.

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