Angioedema of the tongue, oral mucosa, and pharynx is a highly visible and easily diagnoseable side effect of Angiotensin-converting enzyme inhibitors (ACEI). Angioedema of the small bowel is a rarer, and underrecognized, adverse event that may present as a diagnostic challenge due to its nonspecific symptoms and lack of visibility, and because of a general lack of awareness of it among physicians. Failure to consider ACEI-induced angioedema of the small bowel in differential diagnoses may result in unnecessary interventions and delay of treatment. METHODS: We describe the case of a 61-year-old female who was diagnosed with ACEI-induced angioedema of the small intestine after several repeated evaluations. We undertook a literature search to help provide diagnostic, treatment, and management suggestions in patients with ACEI-induced angioedema of the small intestine. RESULTS AND CONCLUSION: In the literature, we found that age, patient demographics, and careful medical reconciliation, paired with diagnostic clues in radiology, can assist in accurate diagnosis. More broadly, family and emergency medicine physicians, surgeons, radiologists, and internists should be aware of this rare side effect caused by this commonly prescribed medication to avert unnecessary medical treatments and procedures.

The capacity of buffalo milk proteins to release bioactive peptides was evaluated and novel bioactive peptides were identified. The sequential similarity between buffalo milk proteins and their cow counterparts was analysed. Buffalo milk proteins were simulated to yield theoretical peptides via in silico proteolysis. The potential of selected proteins to release specific bioactive peptides was evaluated by the A value obtained from the BIOPEP-UWM database (Minkiewicz et al. in Int J Mol Sci 20(23):5978, 2019). Buffalo milk protein is a suitable precursor to produce bioactive peptides, particularly dipeptidyl peptidase IV (DPP-IV) and angiotensin I-converting enzyme (ACE) inhibitory peptides. Two novel ACE inhibitory peptides (KPW and RGP) and four potential DPP-IV inhibitory peptides (RGP, KPW, FPK and KFTW) derived from in silico proteolysis of buffalo milk proteins were screened using different integrated bioinformatic approaches (PeptideRanker, Innovagen, peptide-cutter and molecular docking). The Lineweaver-Burk plots showed that KPW (IC50 = 136.28 ± 10.77 μM) and RGP (104.72 ± 8.37 μM) acted as a competitive inhibitor against ACE. Similarly, KFTW (IC50 = 873.92 ± 32.89 μM) was also a competitive inhibitor of DPP-IV, while KPW and FPK (82.52 ± 10.37 and 126.57 ± 8.45 μM, respectively) were mixed-type inhibitors. It should be emphasized that this study does not involve any clinical trial.

Introduction: Since the coronavirus disease 2019 (COVID-19) pandemic, the use of angiotensin II receptor blockers (ARBs) in hypertensive patients with COVID-19 has been controversial. Following our previous study, after one year, we intended to extend our sample size and results to investigate the effects of ARBs with both in-hospital outcomes and 7-month follow-up results in patients with COVID-19. Methods: Patients with a diagnosis of COVID-19 who were admitted to Sina Hospital, Tehran, Iran, from February to October 2020 participated in this follow-up cohort study. The COVID-19 diagnosis was based on a positive polymerase chain reaction test or chest computed tomography scan according to guidelines. Patients were followed for disease severity, incurring in-hospital mortality, complications, and 7-month all-cause mortality. Results: We evaluated 1413 patients with COVID-19 in this study. After excluding 124 patients, 1289 including 561(43.5%) hypertensive patients, entered the analysis. During the study, 875(67.9%) severe disease, 227(17.6%) in-hospital mortality, and 307(23.8%) 7-month all-cause mortality were observed. After adjusting for possible confounders, ARB was not associated with severity, in-hospital and 7-month all-cause mortality, and in-hospital complications except for acute kidney injury. Discontinuation of ARBs was significantly associated with higher in-hospital mortality and 7-month all-cause mortality (both P values<0.006). We observed a better 7-month outcome in those who continued their ARBs after discharge. Conclusion: The results of this study, along with the previous studies, provide reassurance that taking ARBs is not associated with the risk of mortality, complications, and poorer outcomes in hypertensive COVID-19 patients after adjustment for possible confounders.

Background: The role of antihypertensive drugs in inducing hyperuricaemia and gout has been a long-term concern in clinical practice. However, clinical studies regarding this issue are limited in number and have yielded inconsistent results. We comprehensively evaluated the association between various antihypertensive drugs and the occurrences of hyperuricaemia, gout and related adverse events (AEs) using the FDA Adverse Event Reporting System (FAERS), aiming to guide the selection of antihypertensive drugs with a goal of minimizing the risk of hyperuricaemia, gout and related AEs. Methods: We used OpenVigil 2.1 to query the FAERS database. Hyperuricaemia, gout and related AEs were defined by 5 Preferred Terms: hyperuricaemia, gout, gouty arthritis, gouty tophus and urate nephropathy. Disproportionality analysis was performed, and a positive signal indicated an association between AEs and antihypertensive drugs. Results: The numbers of antihypertensive drugs with positive signals for hyperuricaemia, gout, gouty arthritis, gouty tophus and urate nephropathy were 46, 66, 27, 8 and 6, respectively. These drugs included diuretics, antihypertensive drugs with central action, α blockers, β blockers, α and β blockers, calcium channel blockers, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, renin inhibitors, vasodilators, and compound preparations. Furthermore, 42 antihypertensive drugs had positive signal for more than one AEs. Conclusion: Our study suggests that some potassium-sparing diuretics, calcium channel blockers and losartan may be associated with increased risk of hyperuricaemia, gout or related AEs, which is inconsistent with most previous studies. Moreover, Our study also suggests that some antihypertensive drugs with central action, α and β blockers, renin inhibitors and vasodilators may be associated with increased risk of hyperuricaemia, gout or related AEs, which has not been reported in previous studies. These findings complement real-world evidence on the potential risks of hyperuricaemia, gout and related AEs associated with antihypertensive drugs.

The new 2021 guidelines of the European Society of Cardiology (ESC) have broken with the old step by step treatment of heart failure and have fundamentally revised the strategy in the pharmacotherapy setting. For patients with heart failure and reduced ejection fraction ≤ 40%, the 4 substance groups angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor-neprilysin inhibitors (ARNI), beta blockers, mineralocorticoid receptor antagonists (MRA) and sodium-glucose transporter 2 (SGLT2) inhibitors are now recommended as early as possible after diagnosis. Completing the substance groups has priority over increasing the dosage of the individual substances. This makes it necessary to rethink current clinical practice, especially as the guidelines are reluctant to give concrete instructions for implementation.

The receptor binding domain (RBD) plays a pivotal role in the viral entry as it enables the engagement of severe acute respiratory syndrome 2 (SARS-CoV-2) with the human angiotensin-converting enzyme 2 (ACE2) receptor for host cell entry. RBD is the major target for developing viral inhibitors and vaccines. Expression of recombinant RBD in E.coli is highly scalable with a low-cost procedure despite its high expression level compared to expression in mammalian and yeast cells. Using an alternative natural adjuvant system instead of alum adjuvant, increased immunogenicity of RBD antigen in serological assay including direct ELISA and surrogate Virus Neutralization Test (sVNT) was demonstrated with high levels of IgGs and neutralizing antibodies in mice sera immunized with RBD:AlSa (Alum and Sodium alginate) formulation. The sVNT is a simple and fast test that can be used instead of the conventional virus neutralization test requiring live virus and BSL3 laboratory to detect total neutralizing antibodies against RBD. Additionally, results showed a safety profile for sodium alginate which supported using it as an alternative natural adjuvant.

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to be a major health problem worldwide. Due to the fast emergence of SARS-CoV-2 variants, understanding the molecular mechanisms of viral pathogenesis and developing novel inhibitors are essential and urgent. Here, we investigated the potential roles of N6,2'-O-dimethyladenosine (m6Am), one of the most abundant modifications of eukaryotic messenger ribonucleic acid (mRNAs), in SARS-CoV-2 infection of human cells. Using genome-wide m6Am-exo-seq, RNA sequencing analysis, and Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 genome editing, we demonstrate that phosphorylated C-terminal domain (CTD)-interacting factor 1 (PCIF1), a cap-specific adenine N6-methyltransferase, plays a major role in facilitating infection of primary human lung epithelial cells and cell lines by SARS-CoV-2, variants of concern, and other coronaviruses. We show that PCIF1 promotes infection by sustaining expression of the coronavirus receptors angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) via m6Am-dependent mRNA stabilization. In PCIF1-depleted cells, both ACE2/TMPRSS2 expression and viral infection are rescued by re-expression of wild-type, but not catalytically inactive, PCIF1. These findings suggest a role for PCIF1 and cap m6Am in regulating SARS-CoV-2 susceptibility and identify a potential therapeutic target for prevention of infection.

A one and a half years old male French bulldog weighing 9.50 kg was presented with the history of inappetence, lethargy, abdominal distension and exercise intolerance since last 2 days. The physical examination was done which revealed normal physiological parameters including temperature, mucus membrane color and capillary refill time except palpable precordial thrills, jugular distension on palpation, tachycardia and systolic murmurs on auscultation. Electrocardiography (ECG) was done which depicted ectopic foci with atrioventricular junctional tachycardia and right ventricular enlargement involving very small inverted P waves, deep S waves in leads I, II, III and augmented vector foot (aVF) and splintered QRS complexes. The dog was undergone chest radiography that revealed right atrial enlargement, increased sternal contact of heart on lateral view and a bulge at 9:00 o'clock to 11:00 o'clock depicted right atrial enlargement on dorso-ventral view. Lastly, echocardiography was done to arrive at a diagnosis confirming the Ebstein's anomaly as a form of tricuspid valve dysplasia including apical displacement of tricuspid valve leaflets, division of right ventricle into atrialized and functional portions, increased displacement index, increased apex-mitral annulus to apex-tricuspid annulus ratio, severe right atrial dilatation and tricuspid regurgitation. The dog was medically treated with diuretics, angiotensin converting enzyme inhibitors and inotropes and the owner was advised to put the dog on low sodium diet for 2 weeks. The dog has resolved clinical signs of right sided heart affection; but, suddenly collapsed at home. The owner denied for the necropsy of dog.

Coronavirus Disease 2019 (COVID-19), has already posed serious threats and impacts on the health of the population and the country's economy. Therefore, it is of great theoretical significance and practical application value to better understand the process of COVID-19 infection and develop effective therapeutic drugs. It is known that the receptor-binding structural domain (SARS-CoV-2 RBD) on the spike protein of the novel coronavirus directly mediates its interaction with the host receptor angiotensin-converting enzyme 2 (ACE2), and thus blocking SARS-CoV-2 RBD-ACE2 interaction is capable of inhibiting SARS-CoV-2 infection. Firstly, the interaction mechanism between SARS-CoV-2RBD-ACE2 was explored using molecular dynamics simulation (MD) coupled with molecular mechanics Poisson-Boltzmann surface area (MM-PBSA) free energy calculation method. The results of energy analysis showed that the key residues R403, R408, K417, and Y505 of SARS-CoV-2 RBD and the key residues D30, E37, D38, and Y41 of ACE2 were identified. Therefore, according to the hotspot residues of ACE2 and their distribution, a short peptide library of high-affinity SARS-CoV-2 RBD was constructed. And by using molecular docking virtual screening, six short peptides including DDFEDY, DEFEDY, DEYEDY, DFVEDY, DFHEDY, and DSFEDY with high affinity for SARS-CoV-2 RBD were identified. The results of MD simulation further confirmed that DDFEDY, DEYEDY, and DFVEDY are expected to be effective inhibitors. Finally, the allergenicity, toxicity and solubility properties of the three peptide inhibitors were validated.

Recent studies have suggested that dipeptidyl peptidase 4 (DPP4) inhibitors increase the risk of development of bullous pemphigoid (BP), which is the most common autoimmune blistering skin disease; however, the associated mechanisms remain unclear, and thus far, no therapeutic targets responsible for drug-induced BP have been identified. Therefore, we used clinical data mining to identify candidate drugs that can suppress DPP4 inhibitor-associated BP, and we experimentally examined the underlying molecular mechanisms using human peripheral blood mononuclear cells (hPBMCs). A search of the US Food and Drug Administration Adverse Event Reporting System and the IBM® MarketScan® Research databases indicated that DPP4 inhibitors increased the risk of BP, and that the concomitant use of lisinopril, an angiotensin-converting enzyme inhibitor, significantly decreased the incidence of BP in patients receiving DPP4 inhibitors. Additionally, in vitro experiments with hPBMCs showed that DPP4 inhibitors upregulated mRNA expression of MMP9 and ACE2, which are responsible for the pathophysiology of BP in monocytes/macrophages. Furthermore, lisinopril and Mas receptor (MasR) inhibitors suppressed DPP4 inhibitor-induced upregulation of MMP9. These findings suggest that the modulation of the renin-angiotensin system, especially the angiotensin1-7/MasR axis, is a therapeutic target in DPP4 inhibitor-associated BP.

Hypertension (HTN) is the leading cause of premature deaths worldwide and the main preventable risk factor for cardiovascular diseases. Therefore, there is a current need for new therapeutics to manage this condition. In this regard, protein hydrolysates containing antihypertensive bioactive peptides are of increasing interest. Thus, agri-food industry byproducts have emerged as a valuable source to obtain these hydrolysates as they are rich in proteins and inexpensive. Among these, byproducts from animal origin stand out as they are abundantly generated worldwide. Hence, this review is focused on evaluating the potential role of chicken slaughterhouse byproducts as a source of peptides for managing HTN. Several of these byproducts such as blood, bones, skins, and especially, chicken feet have been used to obtain protein hydrolysates with angiotensin-converting enzyme (ACE)-inhibitory activity and blood pressure-lowering effects. An increase in levels of endogenous antioxidant compounds, a reduction in ACE activity, and an improvement of HTN-associated endothelial dysfunction were the mechanisms underlying their effects. However, most of these studies were carried out in animal models, and further clinical studies are needed in order to confirm these antihypertensive properties. This would increase the value of these byproducts, contributing to the circular economy model of slaughterhouses.

Kuruma shrimp (Marsupenaeus japonicus) heads, as the main by-product of the seafood processing industry, are rich in underutilized high-quality protein. After papain hydrolysis at 50 °C for 4 h, the protein hydrolysate of shrimp heads was found to show notable antibacterial and angiotensin I-converting enzyme (ACE) inhibitory activities. After purification using two stages of revered-phase high-performance liquid chromatography (RP-HPLC), the antibacterial peptide VTVP and the ACE inhibitory peptide ARL/I were successfully identified from most active fractions by LC-MS/MS. Peptide VTVP was a desirable hydrophobic peptide, with a MIC value in the range from 1.62 to 8.03 mM against all tested pathogens. Peptide ARL/I exhibited potent ACE inhibitory activity, with an IC50 value of 125.58 µM, and was found to be a competitive inhibitor based on the Lineweaver-Burk plot. Moreover, the result of the molecular docking simulation indicated that the interaction binding between ARL/I and ACE was mainly stabilized by hydrogen bonds, as well as forming a coordinate bond with the Zn2+ site. The purified peptides did not show hemolytic activity toward rabbit erythrocytes. To sum up, the bioactive peptides isolated from shrimp heads could be applicable for food or pharmaceutical areas as promising ingredients.

Heart failure (HF) is categorized arbitrarily based on the left ventricular ejection fraction (LVEF) in HF with reduced (HFrEF; LVEF < 40%), mildly reduced (HFmrEF; LVEF 40-49%), or preserved ejection fraction (HFpEF; LVEF ≥ 50%). In this opinion paper, based on (patho)physiological considerations, we contend that the neurohormonal overactivity syndrome (NOHS), which is present in all symptomatic HF patients irrespective of their LVEF, not only contributes to the development of signs and symptoms but it is also a major determinant of patients' outcomes. In this regard, NHOS is the only currently available treatment target in HF and should be combatted in most patients with the combined use of diuretics and neurohormonal inhibitors (β-blockers, angiotensin receptor-neprilysin inhibitor/angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, mineralocorticoid antagonists, and sodium-glucose co-transporter 2 inhibitors). Unfortunately, despite the advances in therapeutics, HF mortality remains high. Probably machine learning approaches could better assess the multiple and higher-dimension interactions leading to the HF syndrome and define clusters of HF treatment efficacy.

Cyclooxygenase 2 (COX2) inhibitors have been demonstrated to protect against hypoxia pathogenesis in several investigations. It has also been utilized as an adjuvant therapy in the treatment of COVID-19. COX inhibitors, which have previously been shown to be effective in treating previous viral and malarial infections are strong candidates for improving the COVID-19 therapeutic doctrine. However, another COX inhibitor, ibuprofen, is linked to an increase in the angiotensin-converting enzyme 2 (ACE2), which could increase virus susceptibility. Hence, inhibiting COX2 via therapeutics might not always be protective and we need to investigate the downstream molecules that may be involved in hypoxia environment adaptation. Research has discovered that people who are accustomed to reduced oxygen levels at altitude may be protected against the harmful effects of COVID-19. It is important to highlight that the study's conclusions only applied to those who regularly lived at high altitudes; they did not apply to those who occasionally moved to higher altitudes but still lived at lower altitudes. COVID-19 appears to be more dangerous to individuals residing at lower altitudes. The downstream molecules in the (COX2) pathway have been shown to adapt in high-altitude dwellers, which may partially explain why these individuals have a lower prevalence of COVID-19 infection. More research is needed, however, to directly address COX2 expression in people living at higher altitudes. It is possible to mimic the gene-environment interaction of higher altitude people by intermittent hypoxia training. COX-2 adaptation resulting from hypoxic exposure at altitude or intermittent hypoxia exercise training (IHT) seems to have an important therapeutic function. Swimming, a type of IHT, was found to lower COX-2 protein production, a pro-inflammatory milieu transcription factor, while increasing the anti-inflammatory microenvironment. Furthermore, Intermittent Hypoxia Preconditioning (IHP) has been demonstrated in numerous clinical investigations to enhance patients' cardiopulmonary function, raise cardiorespiratory fitness, and increase tissues' and organs' tolerance to ischemia. Biochemical activities of IHP have also been reported as a feasible application strategy for IHP for the rehabilitation of COVID-19 patients. In this paper, we aim to highlight some of the most relevant shared genes implicated with COVID-19 pathogenesis and hypoxia. We hypothesize that COVID-19 pathogenesis and hypoxia share a similar mechanism that affects apoptosis, proliferation, the immune system, and metabolism. We also highlight the necessity of studying individuals who live at higher altitudes to emulate their gene-environment interactions and compare the findings with IHT. Finally, we propose COX2 as an upstream target for testing the effectiveness of IHT in preventing or minimizing the effects of COVID-19 and other oxygen-related pathological conditions in the future.

Aortic dilation occurs in patients with repaired tetralogy of Fallot (TOF), but the rate of growth is incompletely characterized. The aim of this study was to assess the rates of growth of the aortic root and ascending aorta in a cohort of pediatric and adult patients with sequential magnetic resonance angiography Magnetic Resonance Imaging (MRI) data. Using serial MRI data from pediatric and adult patients with repaired TOF, we performed a retrospective analysis of the rates of growth and associations with growth of the aortic root and ascending aorta. Patients with pulmonary atresia or absent pulmonary valve were excluded. Between years 2005 to 2021, a total of 99 patients were enrolled. A follow-up MRI was performed an average of 5.9 ± 3.7 years from the initial study. For the cohort aged ≥16 years, the mean rate of change in diameter was 0.2 ± 0.5 mm/year at the ascending aorta and 0.2 ± 0.6 mm/year at the sinus of Valsalva. For the entire cohort, the mean change in cross-sectional area indexed to height at the ascending aorta was 7 ± 12 mm2/m/year and at the sinus of Valsalva was 10 ± 16 mm2/m/year. Younger age was associated with higher rates of growth of the sinus of Valsalva while the use of β blockers or angiotensin-converting enzyme inhibitors was associated with a slower rate of growth. There were no cases of aortic dissection in this cohort. We conclude that serial MRI demonstrates a slow rate of growth of the aorta in the TOF.

SARS-CoV-2 (severe acute respiratory syndrome) is highly infectious and causes severe acute respiratory distress syndrome (SARD), immune suppression, and multi-organ failure. For SARS-CoV-2, only supportive treatment options are available, such as oxygen supportive therapy, ventilator support, antibiotics for secondary infections, mineral and fluid treatment, and a significant subset of repurposed effective drugs. Viral targeted inhibitors are the most suitable molecules, such as ACE2 (angiotensin-converting enzyme-2) and RBD (receptor-binding domain) protein-based inhibitors, inhibitors of host proteases, inhibitors of viral proteases 3CLpro (3C-like proteinase) and PLpro (papain-like protease), inhibitors of replicative enzymes, inhibitors of viral attachment of SARS-CoV-2 to the ACE2 receptor and TMPRSS2 (transmembrane serine proteinase 2), inhibitors of HR1 (Heptad Repeat 1)-HR2 (Heptad Repeat 2) interaction at the S2 protein of the coronavirus, etc. Targeting the cathepsin L proteinase, peptide analogues, monoclonal antibodies, and protein chimaeras as RBD inhibitors interferes with the spike protein's ability to fuse to the membrane. Targeting the cathepsin L proteinase, peptide analogues, monoclonal antibodies, and protein chimaeras as RBD inhibitors interferes with the spike protein's ability to fuse to the membrane. Even with the tremendous progress made, creating effective drugs remains difficult. To develop COVID-19 treatment alternatives, clinical studies are examining a variety of therapy categories, including antibodies, antivirals, cell-based therapy, repurposed diagnostic medicines, and more. In this article, we discuss recent clinical updates on SARS-CoV-2 infection, clinical characteristics, diagnosis, immunopathology, the new emergence of variant, SARS-CoV-2, various approaches to drug development and treatment options. The development of therapies has been complicated by the global occurrence of many SARS-CoV-2 mutations. Discussion of this manuscript will provide new insight into drug pathophysiology and drug development.

One of the most relevant and differentiating aspects provided by the 2021 European Society of Cardiology guidelines for the diagnosis and treatment of acute and chronic heart failure is the retraction of the historical stepped and vertical pharmacological treatment scheme for heart failure with reduced ejection fraction (HFrEF). Subsequently, it was replaced by an updated algorithm that places four therapeutic families in the same initial horizontal step with an equally high degree of recommendation (class I). In this context, these four pillars, which have demonstrated a significant reduction in mortality and hospitalizations in patients with HFrEF, include (1) angiotensin-converting enzyme inhibitors (ACEi)/angiotensin receptor blockers (ARB)/angiotensin II receptor-neprilysin inhibitors (ARNi), (2) beta blockers, (3) mineralocorticoid receptor antagonists (MRA) and (4) sodium-glucose cotransporter 2 inhibitors (SGLT2is) as the main novelty. This manuscript reviews the current therapeutic algorithm with a special focus on the therapeutic value of adding an MRA (still underused in both clinical trials and real world), changing an ACEi/ARB for an ARNi and incorporating an SGLT2i in patients with HFrEF. This article is part of the Emerging concepts in heart failure management and treatment Special Issue: https://www.drugsincontext.com/special_issues/emerging-concepts-in-heart-failure-management-and-treatment.

Among the scorpions found in Brazil, Tityus bahiensis is one of the species that causes most of the reported human accidents. In spite of this important constatation, the venom composition description is not available in the literature. Thus, this venom remains not properly studied, segregating this particular species into an abandoned, forgotten condition. In the present study, chromatographic separation (RP-HPLC-C18) and proteomic analyses were employed to unravel the diversity, complexity, and proportional distribution of the main peptides and proteins found in the scorpion venom. Moreover, sequence analyses and the presence of new isoforms and toxins are discussed based on a database comparison with other Tityus toxins. Our results show the presence of a wide diversity of potassium and sodium channel toxins and enzymes, such as metallopeptidases and hyaluronidases, as previously described for other species. However, the current work also describes for the first time, at the protein level, phospholipase, angiotensin-converting enzyme, cysteine-rich proteins, serine peptidase inhibitors peptides, and antimicrobial peptides. Finally, thorough data analyses allowed the description of the venom toxins distribution regarding their diversity and relative quantity. SIGNIFICANCE: The work presents the first Tityus bahiensis proteome. We have focused on describing the neurotoxin variability in terms of their isoforms/amino acid substitutions. Understanding the natural variations in the toxins' sequences is essential, once the affinity of these peptides to their respective receptors/ionic channels will vary depending on the specific peptide sequences. Moreover, the current study describes some proteins present in the venom, including enzymes being described for the first time in scorpion venoms, such as PLA2 and ACE. Moreover, we describe the individual relative quantity distribution for the different protein classes identified, as well as their variability in the T.bahiensis venom. Finally, this study also reports the development of a simple straightforward chromatographic method for scorpion venom fractionation.