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Factor VIII (HemoRel)

✓ Approved

Reliance Life Sciences Private Limited · F8 · Cell-based Therapies

What is Factor VIII?

Factor VIII is a cell-based therapies developed by Reliance Life Sciences Private Limited. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesHemoRel
CompanyReliance Life Sciences Private Limited
Drug ClassCell-based Therapies
Molecular TargetF8
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

Factor VIII acts on 1 molecular target:

F8coagulation factor VIII (AHF, FVIII)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

Factor VIII is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersFactor VIII deficiency✓ Approved

Related Research Articles

PubMedRadiology case reports2026-07-25

An unusual case of neglected CSOM presenting with perineural spread along seventh/eighth cranial nerves to form cerebellar peduncle abscess: A case report.

Sonker Shailly S, Raj Gaurav G

Chronic suppurative otitis media (CSOM) is a common otologic disorder that may occasionally result in intracranial complications. However, extension of infection into the posterior cranial fossa through the facial (VII) and vestibulocochlear (VIII) nerve complex is exceedingly rare. We report the case of an 18-year-old male with a 7-year history of neglected bilateral ear discharge, hearing impairment, and left-sided lower motor neuron facial nerve palsy who presented with severe headache, vomiting, and seizures. Contrast-enhanced magnetic resonance imaging (MRI) demonstrated findings consistent with labyrinthitis, with contiguous enhancement involving the labyrinth, the VII/VIII cranial nerve complex, and the left middle cerebellar peduncle, where an abscess had developed. High-resolution computed tomography (HRCT) of the temporal bone revealed features of advanced CSOM, extensive osseous destruction, labyrinthine fistula formation, and labyrinthitis ossificans. Notably, no defect was identified in Trautmann's triangle. In the absence of alternative pathways of intracranial extension, perineural spread along the facial and vestibulocochlear nerves was considered the most plausible mechanism of infection dissemination. This case highlights a rare route of intracranial spread of otogenic infection through the VII/VIII cranial nerve complex, culminating in cerebellar peduncle abscess formation. Awareness of this uncommon pathway is important for early diagnosis and management of atypical intracranial complications of CSOM.

PubMedThe American surgeon2026-07-25

Blunt Splenic Injury in Hemophilia A: Embolic Agent Selection When Hemostasis Cannot be Assumed.

Akalın Çağrı Ç, Akkaya Hüseyin H

Blunt splenic injury in a patient with hemophilia A presents a dilemma that has traditionally been settled by splenectomy. Removing the spleen leaves a patient already prone to bleeding without its immune function, and the factor VIII (FVIII) exposure that open surgery requires is itself a recognized trigger for inhibitor formation. In the general trauma population, nonoperative management is now the standard for hemodynamically stable patients: observation suffices in most, and splenic artery embolization is reserved for higher-risk injuries. Patients with inherited coagulopathy, however, sit outside the trials and guidelines that built this paradigm. We present a 66-year-old man with mild hemophilia A (FVIII activity 13%), cardiac comorbidity, and a plasma allergy who sustained a blunt splenic laceration graded as American Association for the Surgery of Trauma (AAST) Grade II. No interim computed tomography was obtained; by hospital day 3, selective angiography showed an arteriovenous fistula that had been absent at presentation, a delayed vascular complication of the original injury. Coils and particulate agents failed to achieve occlusion, whereas a 1:3 N-butyl cyanoacrylate (NBCA)-lipiodol mixture produced immediate and complete vessel sealing via coagulation-independent polymerization. Using this case as an anchor, we review nonoperative management of splenic injury across inherited and acquired coagulopathy, compare coagulation-dependent and coagulation-independent embolic agents, and propose a multidisciplinary approach spanning factor replacement, agent selection, and immunoprophylaxis for this underserved population.

PubMedJPRAS open2026-07-25

DIEP reconstruction in a patient with Factor V Leiden deficiency: A case report and literature review.

Quinn Olivia O, Bhatti Sumbal S, Rosich-Medina Anais A

We report a 63-year-old female with Factor V Leiden deficiency who underwent a left delayed DIEP flap reconstruction with contralateral symmetrising breast reduction following mastectomy. Hypercoagulable disorders are theorised to increase flap failure risk. Current evidence and operative guidance are limited. A focused review of the literature is provided.

PubMedBlood2026-07-25

Factor V is an anticoagulant of the extrinsic pathway of coagulation and modifier of thrombin generation in hemophilia A.

Jewell Megan M, Baird Christine H CH, Thornhill Dianne D, Ashour Zaina Z et al.

Factor V (FV) links procoagulant amplification to anticoagulant feedback, but how FV limits tissue factor-initiated coagulation are not fully defined. We hypothesized that procofactor FV downregulates factor X (FX) activation by tissue factor:factor VIIa (TF:FVIIa), independently of tissue factor pathway inhibitor α (TFPIα), and that this mechanism is especially important in hemophilia. Thrombin generation was measured in FV/FVIII‑immunodepleted plasma and synthetic plasma while titrating FV, with TFPIα removed, blocked, or re-added. TF:FVIIa activation of FX was measured on phosphatidylserine‑containing or phosphatidylserine‑free liposomes with antibodies against the FV light chain and C2 domain. FV and TFPIα levels modulated thrombin generation in plasma from people with hemophilia A. In TF‑initiated coagulation lacking TFPIα, thrombin generation peaked at 2 nM FV and decreased as FV increased; at 20 nM FV (normal concentration), peak thrombin and thrombin generation rate were reduced by up to 50-80%, with larger effects at low FVIII. In purified TF:FVIIa assays, FV reduced FX activation by ~80% at physiologic concentration and inhibited FX activation on TF-expressing fibroblasts. Increasing PS content enhanced FX activation and increased the FV-sensitive component, while blocking the FV light chain or C2 domain partially relieved inhibition. In hemophilia A plasma, higher FV was associated with longer lag time and time-to-peak, and lower peak thrombin independent of TFPIα. Thus, FV is an endogenous anticoagulant that inhibits TF-initiated coagulation by limiting FX activation by TF:FVIIa through a membrane-dependent mechanism. This mechanism refines models of coagulation initiation and may help explain how FV variation contributes to bleeding and thrombosis.

PubMedJournal of hepato-biliary-pancreatic sciences2026-07-25

Comment on "Stump Ischemia Is a Possible Risk Factor for Late-Onset Pancreatic Fistula After Distal Pancreatectomy".

Xu Shitang S

PubMedJournal of pediatric nursing2026-07-25

The development of the developmental dysplasia of the hip awareness scale and examination of its psychometric properties.

Yolcu Betül B, Tiryaki Öznur Ö

This study aimed to develop the "Developmental Dysplasia of the Hip Awareness Scale (DDHAS) and assess its psychometric properties. The methodological study included mothers (n = 400) with infants aged 0-2 months. Data were collected using a socio-demographic information form and the draft of the DDHAS. Factor analysis and reliability analyses were performed to evaluate the scale's psychometric properties. The data were analyzed using IBM SPSS Statistics 23 and IBM SPSS AMOS 23. Exploratory factor analysis (EFA) and confirmatory factor analysis (CFA) of the scale revealed a structure consisting of 24 items and three sub-dimensions. The factor loadings of the scale were found to be above 0.40. Following CFA, the fit indices were at adequate levels. The Cronbach's alpha for the entire scale was 0.878, while the values for the sub-dimensions ranged from 0.850 to 0.913, indicating good internal consistency. Based on the findings obtained, the DDHAS demonstrated acceptable psychometric properties and may be used as a measurement instrument to assess the level of awareness of developmental dysplasia of the hip among mothers with infants aged 0-2 months. Midwives and nurses can use the Developmental Dysplasia of the Hip Awareness Scale in their clinical practice and training to assess mothers' awareness of developmental dysplasia of the hip. It is also recommended that the scale be adapted and validated for use in different cultural contexts.

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