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antithrombin III (Atenotiv / ATenativ / ATnativ)

✓ Approved

Pfizer, Inc. · SERPINC1 · Cell-based Therapies

What is antithrombin III?

antithrombin III is a cell-based therapies developed by Pfizer, Inc.. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesAtenotiv, ATenativ, ATnativ
CompanyPfizer, Inc.
Drug ClassCell-based Therapies
Molecular TargetSERPINC1
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Pfizer, Inc.

Mechanism of Action

Molecular Targets

antithrombin III acts on 1 molecular target:

SERPINC1serpin family C member 1 (ATIII, AT3D)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

antithrombin III is developed for 3 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersAntithrombin III deficiency✓ Approved
Vascular disordersThrombosis✓ Approved
Surgical and medical proceduresAdjuvant therapy✓ Approved

Related Research Articles

PubMedJournal of clinical and experimental hepatology2026-05-25

Genome-Wide Association Study to Identify Novel Genetic Variants Associated With Primary Budd-Chiari Syndrome.

Kumar Sonu S, Biswas Sagnik S, Agarwal Samagra S, Agarwal Ayush A et al.

Primary Budd-Chiari syndrome (BCS) is a rare hepatic vascular disorder characterized by hepatic venous outflow obstruction involving the hepatic veins and/or inferior vena cava. Marked geographic variation in vascular anatomy and prothrombotic profile suggests an underlying genetic predisposition. This study aimed to identify genetic variants associated with primary BCS using genome-wide association study (GWAS) and to characterize implicated biological pathways. In a case-control study (June 2020-May 2022), 310 adults with primary BCS and 312 age- and sex-matched healthy controls were recruited; after quality control, 262 cases and 265 controls were included. Whole-blood DNA underwent high-density single-nucleotide polymorphism (SNP) genotyping on an Illumina bead-array platform. SNPs were mapped to genes and assessed using gene ontology, pathway, and tissue-expression analyses. Overall, 7,78,783 high-quality SNPs were analyzed; 1549 were associated with BCS at P < 0·05 and 340 lead SNPs at P < 0·001. Fifteen top SNPs (P < 5 × 10-5) were predominantly intronic, intergenic, or regulatory and mapped to loci including rs13164180, rs6883351, rs1558294, rs2656107, rs1413229, rs2903138, rs4919217, rs11948339, rs6936121, rs62218439, rs12966305, rs1609245, rs965428, rs697957, and rs34176204. Functional enrichment implicated extracellular matrix constitution and remodeling, cell-cell junctions, focal adhesion, and vasoconstriction pathways, with no overlap between lead SNPs and canonical hypercoagulable genes (protein C/S, antithrombin III, Factor V, JAK2, and calreticulin). This GWAS study in primary BCS identifies novel germline loci predominantly in noncoding and regulatory regions, implicating extracellular matrix remodeling, vascular tone, and cell-adhesion pathways rather than classical thrombophilia genes, and supports further functional studies to refine genetic risk stratification.

PMID 42181163
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PubMedInternational journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group2026-05-25

Diagnostic utility of the platelet-to-thrombin-antithrombin complex ratio in heatstroke: a single-center retrospective analysis.

He Long-Ping LP, Yu Shi-Kai SK, Lin Qing-Wei QW, Zhong Lin-Cui LC et al.

To assess the discriminatory performance of the platelet-to-thrombin-antithrombin complex ratio (PLT/TAT) for differentiating heatstroke from heat exhaustion and to explore its association with 28-day prognosis and disease severity. This retrospective study analyzed 100 heat illness patients from 2018 to 2025, including 45 with heat exhaustion and 55 with heatstroke. Baseline and admission laboratory data were analyzed using RF, LASSO and SVM-RFE to discern heatstroke risk factors. Diagnostic accuracy of PLT/TAT was evaluated via ROC curve analysis, complemented by Kaplan-Meier and Spearman analyses. LASSO, RF, and SVM-RFE analyses identified PLT/TAT, MYO, GCS, Cr, PLT, TAT, PIC, and Lac as heatstroke predictors. The AUC for PLT/TAT in diagnosing heatstroke was 0.938 (95% CI: 0.893-0.982, p < 0.001). At a threshold value of 30.1, the sensitivity and specificity were 86.7% and 89.1%, respectively. Patients with a PLT/TAT ratio below 30.1 exhibited a 5.826-fold increased risk of mortality compared to those with a PLT/TAT ratio above 30.1. Spearman correlation analysis demonstrated a negative correlation between PLT/TAT and Lac (r = -0.519, p < 0.001) and a positive correlation with the GCS score (r = 0.689, p < 0.001), the PLT/TAT ratio exhibited significant negative correlations with ALT (r = -0.614, p < 0.001), AST (r = -0.713, p < 0.001), Cr (r = -0.499, p < 0.001), CK (r = -0.445, p < 0.001) and DIC score(r = -0.764, p < 0.001). The group with PLT/TAT < 30.1 showed significantly elevated Lac levels and reduced GCS score compared to the group with PLT/TAT > 30.1 (p < 0.001). The PLT/TAT ratio was associated with heatstroke severity and 28-day survival, making it a promising adjunctive biomarker for diagnosis and risk stratification.

PMID 42178783
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PubMedbioRxiv : the preprint server for biology2026-05-25

A sensitized model of thrombosis validates known multigenic relationships and suggests novel modifiers of hemostasis.

Grzegorski Steven J SJ, Liu Yang Y, Richter Catherine E CE, Yaman Murat M et al.

Venous thromboembolism is a major cause of morbidity and mortality. Despite identification of risk factors, not all individuals with thrombophilia develop thrombosis. Understanding the multigenic factors modifying this incomplete penetrance would help guide patient care. The zebrafish has a conserved hemostatic system and is amenable to large genetic studies. Loss of antithrombin III (At3) in zebrafish leads to an early consumptive coagulopathy and lethality in adulthood. Using this genetic background as a sensitized model we performed a dominant unbiased genome-wide N-ethyl-N-nitrosourea (ENU) mutagenesis screen followed by whole genome sequencing (WGS). We used survival studies, laser-mediated endothelial injury, and ex vivo protein assays to validate hits. ENU-treated at3 +/- males were crossed with at3 +/- females to produce 4,030 total offspring (1.5x genome coverage). Four permanent lines transmitting a survival benefit beyond 7 months were identified and sequenced. A candidate screen of 63 known coagulation-related loci revealed a missense mutation, C504F, in a highly conserved residue of the prothrombin ( F2 ) heavy chain, which was validated through genetic and biochemical studies. Evaluation of UK Biobank electronic health record (EHR) data was underpowered to detect interactions between F2 and AT3 due to minmal deleterious mutations. Mutations produced through genome editing revealed that heterozygosity for factor X and plasminogen also modified at3 -/- , resulting in reduced lethality. The three remaining lines had no coagulation-related variants segregating with survival, suggesting the presence of novel modifier loci. Unbiased genome-wide screening identified a modifier of thrombosis. This demonstrated that re-balancing of hemostasis to mitigate thrombosis is conserved in zebrafish, including an unexpected role for fibrinolysis. This interaction was not detected even in a large human dataset, establishing the continued benefit of the zebrafish model. Finally, we found evidence for novel loci outside of the canonical coagulation cascade that may be new targets for diagnosis or treatment.

PMID 42182511
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PubMedThe Journal of craniofacial surgery2026-05-25

Impact of Correcting Skeletal Facial Pattern Types II and III on Quality of Life After Orthognathic Surgery.

da Silva Alexandre Augusto Ferreira AAF, Pereira Max Domingues MD

To evaluate quality of life (QoL) after orthognathic surgery according to the skeletal facial profile pattern and to identify whether the surgical site in the maxilla, mandible, or both influences QoL. Fifty adult patients were analyzed according to the facial profile pattern of the deformity and divided into 2 groups: facial pattern II (24 patients) and III (26 patients). At predetermined time points (T0: preoperative; T1: 3 mo postoperatively; and T2: 6 mo postoperatively), patients completed the Orthognathic Quality of Life Questionnaire (OQLQ) and the Oral Health Impact Profile Questionnaire (OHIP-14). At T0, in the total sample, facial pattern II showed higher QoL compared with facial pattern III (P<0.05). At T2, no difference was observed between the groups; however, the mean reductions in OQLQ and OHIP-14 scores from T0 to T2 were greater in facial pattern III across the total sample. For each group, the reduction in scores in both questionnaires from T0 to T2 was significant (P<0.001). The standardized response mean (SRM) was high and demonstrated large changes for most outcomes, demonstrating that both questionnaires showed substantial improvement in QoL. Facial pattern III showed a higher SRM than facial pattern II, suggesting a greater impact. Within each group, no differences were observed in OQLQ and OHIP-14 scores that influenced QoL related to unimaxillary or bimaxillary surgeries (P>0.05). Facial patterns II and III patients show improvements in QoL after orthognathic surgery. However, because facial pattern III patients present poorer QoL before surgery, they tend to experience greater improvement than facial pattern II patients. QoL is not influenced by whether the surgery is unimaxillary or bimaxillary surgery in either pattern II or III patients.

PMID 42183621
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PubMedbioRxiv : the preprint server for biology2026-05-25

Antiphage defence systems Druantia III and Zorya II synergise via shared DNA intermediates in a phage-specific manner.

Wu Yi Y, Zhang Zhiying Z, Garushyants Sofya K SK, Weigele Peter R PR et al.

Most bacteria encode multiple antiphage defence systems, but how these systems interact, remains poorly understood. Here, we define the mechanism of Druantia III and explore its synergy with Zorya II. Druantia III is a late-acting defence where DruH is the likely infection sensor and DruE is a helicase-nuclease effector that engages ssDNA-containing replication intermediates. Druantia III and Zorya II are each sensitive to the loss of RecD, whereas their synergy requires an intact RecBCD complex, indicating that the combined response depends on a shared DNA-processing hub. During T3 infection, Zorya apparently preserves this hub by limiting accumulation of the phage RecBCD-inhibitor Gp5.9, whereas DruE together with RecBCD promote the formation of DNA structures permissive for ZorE cleavage. During Bas37 infection, Druantia provides the dominant pathway and recruits ZorE in a non-canonical, ZorAB-independent manner. These findings show how shared DNA intermediates can connect defence systems into a coordinated antiphage response.

PMID 42182148
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PubMedbioRxiv : the preprint server for biology2026-05-25

HS3ST1 regulates pulmonary inflammation and is a determinant of clinical outcomes after trauma and hemorrhagic shock.

Mokhtari Ava K AK, Cotton Madeline E ME, Thomas Kimberly A KA, Chitrakar Alisha A et al.

Mechanisms that promote organ injury after trauma and hemorrhagic shock (T/HS) remain poorly defined. Endothelial heparan sulfates with a 3-O-sulfate (3-OS) modification, controlled by the HS3ST1 gene, have anticoagulant and anti-inflammatory properties through their interaction with antithrombin. Our objective was to determine whether HS3ST1 deficiency drives organ injury and poor outcomes after T/HS. Hs3st1 -/- and wild-type (WT) mice were subjected to T/HS followed by resuscitation with lactated ringer's (LR) or fresh frozen plasma (FFP). While no differences were observed between WT and Hs3st1 -/- LR resuscitated mice, lung injury and leukocyte infiltrates were significantly increased in FFP resuscitated Hs3st1 -/- compared to WT mice. In vitro, leukocyte slow rolling and adherence was increased in HS3ST1 KO compared to WT cells. Among 472 T/HS patients, of which 31 (7%) were homozygous for the rs16881446 variant allele (GG), the number of ventilator free days was lower, and mortality was significantly higher in AG and GG patients. The rs16881446 genotype was independently associated with mortality. In conclusion, HS3ST1 deficiency mitigates organ protection from FFP resuscitation, partly through mediating EC:leukocyte engagement, and predicts mortality after T/HS. These findings identify a novel therapeutic target and prognostic tool that can be leveraged towards improved risk stratification after trauma.

PMID 42182247
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