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snake venom antibody-2 (ViperaTAb)

✓ Approved

MicroPharm · Polyclonal Antibodies · Polyclonal Antibodies

What is snake venom antibody-2?

snake venom antibody-2 is a polyclonal antibodies developed by MicroPharm. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesViperaTAb
CompanyMicroPharm
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, MicroPharm

Therapeutic Indications

snake venom antibody-2 is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Injury, poisoning and procedural complicationsVenom poisoning✓ Approved

Related Research Articles

PubMedHaematologica2026-10-15

Cord blood-derived natural killer cells engineered with a novel, highaffinity chimeric antigen receptor can eliminate acute myeloid leukemia cells with minimal C-type lectin-like molecule-1 expression.

Suga Makiko M, Kida Shuhei S, Mizutani Yo Y, Kogue Yosuke Y et al.

CAR NK cell therapy is expected to be developed to treat acute myeloid leukemia (AML). C-type lectin-like molecule 1 (CLL-1) is a candidate target. However, AML cells with minimal CLL-1 expression (CLL-1dim) may not be eliminated by CAR NK cells. Here we demonstrate that cord blood (CB)-derived NK cells transduced with a novel high-affinity CAR that recognizes CLL-1 can eliminate CLL-1dim AML cells. A newly established anti- CLL-1 monoclonal antibody (mAb) designated as 2-23 exhibits a higher affinity for CLL- 1 than the widely used anti-CLL-1 mAb M26. CB-derived NK cells transduced with a CAR derived from 2-23, but not M26, killed CLL-1dim AML cells in vitro. Additionally, treatment with 2-23 CAR NK cells, but not M26 CAR NK cells, significantly enhanced the survival of the mice transplanted with CLL-1dim AML cells in vivo. Furthermore, in AML patient-derived xenograft models, the 2-23 CAR NK cells expanded robustly, persisted, and eradicated AML cells.

PMID 42876290
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-15

Fc-Dependent Targeting of the GAS6-MERTK Axis With Monoclonal and Bispecific Antibodies Overcomes Drug Resistance Across EGFR Mutations in Exons 19, 20, and 21.

Giri Suvendu S, Selvadurai Boobash Raj BR, Gupta Nitin N, Simoni-Nieves Arturo A et al.

Resistance of lung cancer to EGFR-targeting tyrosine kinase inhibitors (TKIs) like osimertinib frequently results from secondary mutations or activation of bypass signaling pathways. Re-analysis of clinical data unveiled elevated expression of GAS6 and its receptor MERTK in lung cancer patients developing resistance to osimertinib. This implied that the GAS6-MERTK axis could represent a therapeutic vulnerability. Functionally, GAS6 overexpression enhanced cancer cell survival, whereas a new anti-GAS6 antibody delayed tumor relapses in xenograft models. Similarly, ablation of MERTK sensitized lung cancer cells to osimertinib, revealing a bypass crosstalk between EGFR and MERTK, likely taking place within caveolae. An anti-MERTK antibody was generated, and a bispecific antibody, Bis-EM, targeting both EGFR and MERTK, was designed. Bis-EM promoted the degradation of both receptors and displayed the capacity to promote immune-mediated cell killing. In combination with TKIs, concurrent antibody-mediated inhibition of MERTK and EGFR suppressed the growth of TKI-resistant spheroids. Co-treatment with Bis-EM and TKIs delayed tumor relapses in an Fc-dependent manner across patient-derived xenografts harboring clinically challenging EGFR exon 20 insertions and other mutations. Collectively, these findings identify the GAS6-MERTK axis as an important driver of drug resistance and provide a strong rationale for the clinical development of Bis-EM.

PMID 42875888
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PubMedCommunications biology2026-10-15

Selective inhibition of IL-6 trans-signalling reveals distinct mechanisms of human classic and trans-signalling receptor-complex formation.

Rieneck Emelie E, Haak Jan René JR, Asgarov Kamal K, Pallandre Jean-René JR et al.

The cytokine interleukin-6 orchestrates inflammation through two distinct pathways of receptor activation: anti-inflammatory classic signalling via membrane-bound interleukin-6 receptor and pro-inflammatory trans-signalling via soluble interleukin-6 receptor. Current interleukin-6-targeted therapies block both pathways, thereby disrupting essential homeostatic functions initiated by classic signalling. We here show a high-affinity, human-specific antibody that selectively inhibits interleukin-6 trans-signalling. This antibody maintains classic signalling-induced expression of hepatic acute phase genes while completely blocking trans-signalling-induced activation of endothelial cells. By targeting the domain D2 of membrane-bound and soluble human interleukin-6 receptor, the antibody selectively prevents formation of the trans-signalling receptor complex without interfering with ligand binding. This selective blockade demonstrates that human interleukin-6 classic and trans-signalling proceed through distinct receptor assemblies. Our findings describe mechanistic insight into interleukin-6 receptor assembly and provide a strategy to suppress inflammatory interleukin-6 activity while preserving regenerative and anti-inflammatory signalling, thus offering both conceptual and potential therapeutic advances in the targeted modulation of cytokine signalling networks.

PMID 42875473
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PubMedFrontiers in pharmacology2026-10-15

Monoclonal antibodies associated IgA nephropathy or other nephropathies.

Miedziaszczyk Miłosz M, Kosiorowski Gracjan G, Kubasik Janusz J, Grabowski Tomasz T et al.

The use of monoclonal antibodies (mAbs) has revolutionized the treatment of autoimmune, inflammatory, and neoplastic diseases. However, accumulating evidence indicates that biologic therapies may be associated with renal adverse events, including various types of glomerulonephritis. The aim of this review was to summarize all reports available in the scientific literature regarding the occurrence of IgA nephropathy after monoclonal antibody treatment. Additionally, the risk of other glomerulonephritis after biologic therapy was discussed. IgA nephropathy (IgAN) is the most commonly reported glomerular lesion associated with monoclonal antibody therapy, particularly with TNF-α inhibitors such as infliximab, adalimumab, golimumab, and etanercept, as well as with immune checkpoint inhibitors targeting the PD-1 (pembrolizumab, nivolumab) and interleukin (ustekinumab) pathways. Proposed mechanisms include immune dysregulation with a shift toward Th2 and Th17-dependent responses, increased production of galactose-deficient IgA1, complement activation, formation of circulating immune complexes, and loss of immune tolerance. In some cases, drug discontinuation and glucocorticoid therapy have resulted in partial or complete disease remission, although progression to end-stage renal disease has also been reported. Due to the potential severity of these complications, initial and periodic monitoring of renal function and urinalysis are recommended in patients receiving monoclonal antibody therapy. Early recognition of renal involvement and prompt treatment modification can improve prognosis.

PMID 42876810
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PubMedBiochemistry and biophysics reports2026-10-15

Phospholipase A2 enhances the cytotoxic activity of membranolytic peptide Polybia MP1 in some breast epithelial cells.

Pramanik Arindam A, Wang Dapeng D, Kobza Dagmara D, Reed Lewis P LP et al.

MP1, a peptide from the venom of the wasp Polybia paulista, has been investigated for anti-microbial and anti-cancer properties. The peptide binds and disrupts external-facing lipid membranes of various cell types, thereby reducing cellular viability, with some reported selectivity for cancer cells. The molecular basis of selectivity is poorly understood. We have assessed MP1 activity in a panel of human cells, with the aims of establishing the types most suited to development of future MP1-derived therapies and identifying molecular factors influencing responses. Cellular viability was tested in 64 cancer cell lines after treatment with MP1 to determine IC50 values. These varied by 8.5-fold across the panel, with blood cancer lines proving most sensitive and colorectal cancer lines most resistant, and breast cells showing the greatest variance. Transcriptome data were downloaded for cell lines and relationships between expression levels of each individual gene and IC50 values were assessed using linear regression. 67 genes demonstrated significant correlations after correction for multiple testing, within which lipases were significantly over-represented. The impact on viability of exogenous phospholipase A2 with and without MP1 was tested in four different breast epithelial cell lines that represented a wide range of intrinsic sensitivities to MP1 alone. Phospholipase A2 had little significant influence on viability alone, but caused potent and dose-dependent potentiation of MP1-induced cytotoxicity in two of the four cell lines tested. We conclude that phospholipase A2 and MP1 act together on some breast cancer cell membranes, and that this combinatorial influence could impact on future development of MP1 as a cancer therapy.

PMID 42876472
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PubMedNature communications2026-10-15

Angiotensin II exacerbates intracerebral hemorrhage in mice via heparin-like antithrombin activation and coagulation dysfunction.

Wang Shaoying S, Xue Min M, Yan Musan M, Liu Chuanfeng C et al.

Hypertension has paradoxical prothrombotic-hemorrhagic predisposition toward cerebral infarction and intracerebral hemorrhage (ICH), but the mechanism remains poorly understood. We observed Angiotensin II (Ang II) inhibited coagulation by activating antithrombin through heparin-like acceleration of antithrombin-thrombin interaction. Ang II allosterically modulates the 386-397 loop of antithrombin to enhance thrombin inhibition. In vivo, single injection of Ang II inhibited coagulation, alleviating thrombosis and aggravating ICH. Conversely, anti-Ang II monoclonal antibody promoted coagulation, aggravating thrombus formation and alleviating ICH. Notably, the blockage or deficiency of Ang II receptor had no significant effect on the alleviated thrombus formation or aggravated hemorrhage elicited by Ang II, suggesting the phenotypes were independent of Ang II receptor. In hypertensive mice, anti-Ang II monoclonal antibody significantly promoted coagulation and ameliorated ICH. These results identify Ang II as a key coagulation regulator with heparin-like function, suggesting that targeting Ang II-coagulation pathway could be a novel strategy to mitigate cerebral bleeding.

PMID 42875448
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