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* 3F1 treatment effectively prevented dental caries by controlling S. mutans in a rat caries model without perturbing the oral microbiota. At 5 micromolars (μM)] , the small molecule annotated 3F1 dispersed 50% of the established S. mutans biofilm but did not disperse biofilms formed by the commensal species Streptococcus sanguinis or Streptococcus gordonii. 3F1 dispersed S. mutans biofilms independently of biofilm-related factors such as antigen I/II and glucosyltransferases. 3F1 was able to effectively reduce dental caries in vivo without affecting the overall oral microbiota shaped by the intake of dietary sugars, suggesting that the pathogenic biofilm-specific treatment is a viable strategy for disease prevention. Streptococcus mutans metabolizes sucrose to initiate biofilm formation on the tooth surface and consequently produces lactic acid to degrade the tooth’s enamel. Persistence of S. mutans biofilms in the oral cavity can lead to tooth decay.  

* Activated Charcoal also known as activated carbon, is a medication used to treat poisonings that occurred by mouth. To be effective it must be used within a short time of the poisoning occurring, typically an hour. It does not work for poisonings by cyanide, corrosive agents, iron, lithium, alcohols, or malathion. Other uses include inside hemoperfusion machines. Common side effects include vomiting, black stools, diarrhea, and constipation. The more serious side effect, pneumonitis, may result if aspirated into the lungs. Gastrointestinal obstruction and ileus are less common but serious adverse effects. Use in pregnancy and breastfeeding is safe. Activated charcoal works by adsorbing the toxin. While charcoal has been used since ancient times for poisonings, activated charcoal has been used since the 1900s. It is on the World Health Organization's List of Essential Medicines. Activated charcoal is used to treat many types of oral poisonings such as phenobarbital and carbamazepine. It is not effective for a number of poisonings including: strong acids or bases, iron, lithium, arsenic, methanol, ethanol or ethylene glycol. Although activated charcoal is the most commonly used agent for GI decontamination in poisoned patients, medical professionals use discretion when determining whether or not its use is indicated. In a study of acute poisonings from agricultural pesticides and yellow oleander seeds, the administration of activated carbon did not affect survival rates.

* ADX71441 is a novel, potent and selective GABAB positive allosteric modulator PAM. In rodent trials caused significant reductions in alcohol intake (up to 65% with the highest dose of 200mg/kg). The drug potently reduced motivation to drink and alcohol-seeking behaviours, suggesting inhibition of alcohol-induced dopamine response and therefore reduced addiction. ADX71441 also caused a significant reduction in alcohol-seeking caused by alcohol-predictive environments and exposure to a stress, suggesting therapeutic use in preventing alcohol use disorder relapse as more than 50% of patients relapse in only 3 months. Preclinical studies suggest the superiority of GABAB PAMs in terms of efficacy to side effects. ADX71441 is an experimental therapy with the potential to slow the progression of nerve damage in people who have Charcot-Marie-Tooth disease, or CMT. Some people with CMT have an extra copy of a gene that codes for peripheral myelin protein 22, or PMP22. PMP22 is necessary for the production of myelin, an insulating layer around nerve cells that promotes the transmission of nerve signals. Too much PMP22 gums up the works, however, ultimately causing the nerve damage associated with CMT. One strategy for slowing the damage is decreasing the amount of PMP22 in nerve cells. Gamma-aminobutyric acid, or GABA, inhibits nerve signal transmission. It does this by reducing the activity of nerve cells when it binds to its GABA receptor. Scientists think that the activation of GABA-B receptors reduces the PMP22 gene’s production of myelin protein. ADX71441 is designed to modify the activity of GABA-B receptors to reduce the protein’s  production. ADX71441 reduced the signs of bladder overactivity in both models of OAB, suggesting that the GABAB PAM approach has potential for the pharmacological treatment of OAB. Overactive bladder (OAB) is a common, chronic and debilitating disorder characterized by urinary urgency often accompanied by incontinence (involuntary urine leakage), frequency (≥8 micturition in 24 h) and nocturia (≥1 awakening per night to void). The GABAB receptor agonist baclofen reduces urethral resistance and detrusor overactivity in patients with spasticity. However, baclofen's side effects limit its use for the treatment of overactive bladder (OAB).  ADX71441 showed efficacy in the marble burying and elevated plus maze tests relevant for anxiety-like supporting and expanding earlier evidence of the broad anxiolytic-like properties of the target.  Acute ADX71441 reduced visceral pain in the acetic acid (AA) writhing test and also reduced chronic pain in the monosodium iodoacetate (MIA)-induced model of osteoarthritis, after acute and subchronic administration regimens.

* Alaproclate (A03), a known selective serotonin reuptake inhibitor, induced dose-response increases of neuroprotective SirT1 in N2a cells stably expressing full-length ApoE4 with an EC 50 of 2mM. Moreover, A03 increased SirT1 levels in ApoE4-transfected human A172 glioblastoma cells. In 5XFAD-ApoE4 AD model mice, subcutaneous administration of A03 (10 mg/kg/day) for 56 days increased SirT1 levels in the hippocampus and elicited cognitive improvement while inducing no observed toxicity. In addition, pharmacokinetic study shows that A03 is orally bioavailable and brainpenetrant. The SirT1 enhancing effects of A03 may decrease acetylated tau levels and abrogate tau pathology, which needs direct evidence in the future studies. Used for tauopathies in neurodegenerative diseases.

* Anakinra is a biopharmaceutical medication used to treat rheumatoid arthritis, cryopyrin-associated periodic syndromes, familial Mediterranean fever, and Still's disease. It is a recombinant and slightly modified version of the human interleukin 1 receptor antagonist protein. Anakinra is administered by subcutaneous injection. It is used as a second line treatment to manage symptoms of rheumatoid arthritis after treatment with a disease-modifying antirheumatic drug (DMARD) has failed. It can be used in combination with some DMARDs. It is used to treat anyone from infants to adults with a cryopyrin-associated periodic syndrome, including neonatal-onset multisystem inflammatory disease. It also appears to be effective in treating macrophage activation syndrome (MAS), a form of cytokine storm. It is used off label to treat Schnitzler's syndrome. It has been shown to help treat secondary hemophagocytic lymphohistiocytosis (HLH) especially in pediatric patients with other rheumatological disorders. It was not tested in pregnant women, but appeared to be safe in animal studies. It should not be used in people who have active infections or latent tuberculosis, who have low white blood cells counts, or who are taking TNF inhibitors. More than ten percent of people taking Anakinra have injection site reactions, headaches, and have increased levels of cholesterol in their blood. Between one and ten percent of people have severe infections, decreased white blood cells, or decreased platelets. It is unclear if taking Anakinra increases the risk of getting cancer; studies are complicated by the fact that people with rheumatoid arthritis are already at higher risk of getting cancer. Anakinra is associated with a low rate of serum enzyme elevations during therapy and with rare instances of clinically apparent, acute liver injury. It was approved in 2020, for the treatment of patients with deficiency of interleukin-1 receptor antagonist, a very rare genetic inflammatory condition resembling an infection throughout the body or a bone infection that happens in newborns during the first days of life.

* Aviptadil ( RLF 100, DK 1000 ) is an injectable synthetic formulation of human vasoactive intestinal peptide (VIP). VIP was discovered in 1970, and has been used to treat various inflammatory conditions, such as acute respiratory distress syndrome (ARDS), asthma and chronic obstructive pulmonary disease (COPD). Studies have found that aviptadil may be beneficial for severely ill patients with COVID-19 related ARDS. COVID-19-related death is primarily caused by Acute Respiratory Distress Syndrome (ARDS). The trigger for ARDS is widely attributed to a cytokine storm in the lungs, in which the virus causes release of inflammatory cytokines. As a result, alveolae of the lungs fill with fluid and become impermeable to oxygen, even in the setting of mechanical ventilation. SARS-CoV-2 is known to cause respiratory failure, which is the hallmark of Acute COVID-19. Undesirable effects: Gastrointestinal Disorders – Diarrhea, Vascular disorders – Hypotension, cutaneous flushing, facial flushing & Infusion related reactions.

* Baloxavir marboxil  is an antiviral medication for treatment of influenza A and influenza B flu. It was approved for medical use both in Japan and in the United States in 2018, Baloxavir marboxil was developed as a prodrug strategy, with its metabolism releasing the active agent, baloxavir acid (BXA). BXA then functions as enzyme inhibitor, targeting the influenza virus' cap-dependent endonuclease activity, used in "cap snatching" by the virus' polymerase complex, a process essential to its life-cycle. The most common side effects of baloxavir marboxil include diarrhea, bronchitis, nausea, sinusitis and headache. Baloxavir marboxil is an influenza medication, an antiviral, for individuals who are twelve years of age or older, that have presented symptoms of this infection for no more than 48 hours. The efficacy of baloxavir marboxil administered after 48 hours has not been tested. Baloxavir marboxil is an influenza medication, an antiviral, for individuals who are twelve years of age or older, that have presented symptoms of this infection for no more than 48 hours. In November 2020, the FDA approved an updated indication to include post-exposure prevention of influenza (flu) for people twelve years of age and older after contact with an individual who has the flu. In October 2019, the FDA approved an updated indication for the treatment of acute, uncomplicated influenza in people twelve years of age and older at risk of influenza complications. Baloxavir marboxil should not be co-administered with dairy products, calcium-fortified beverages, or laxatives, antacids, or oral supplements containing calcium, iron, magnesium, selenium, aluminum or zinc.

* BMS-986020, also known as AM152 and AP-3152 free acid, is a potent and selective LPA1 antagonist. BMS-986020 is in Phase 2 clinical development for treating idiopathic pulmonary fibrosis. BMS-986020 selectively inhibits the LPA receptor, which is involved in binding of the signaling molecule lysophosphatidic acid, which in turn is involved in a host of diverse biological functions like cell proliferation, platelet aggregation, smooth muscle contraction, chemotaxis, and tumor cell invasion, among others. The lysophosphatidic acid receptor, LPA1, has been implicated as a therapeutic target for fibrotic disorders. Lysophospholipids (LPs), including lysophosphatidic acid (LPA), sphingosine 1-phospate (S1P), lysophosphatidylinositol (LPI), and lysophosphatidylserine (LysoPS), are bioactive lipids that transduce signals through their specific cell-surface G protein-coupled receptors, LPA1-6, S1P1-5, LPI1, and LysoPS1-3, respectively. These LPs and their receptors have been implicated in both physiological and pathophysiological processes such as autoimmune diseases, neurodegenerative diseases, fibrosis, pain, cancer, inflammation, metabolic syndrome, bone formation, fertility, organismal development, and other effects on most organ systems.

* Candesartan is an angiotensin-receptor blocker (ARB) that may be used alone or with other agents to treat hypertension. It is administered orally as the prodrug, candesartan cilexetil, which is rapidly converted to its active metabolite, candesartan, during absorption in the gastrointestinal tract. Candesartan lowers blood pressure by antagonizing the renin-angiotensin-aldosterone system (RAAS); it competes with angiotensin II for binding to the type-1 angiotensin II receptor (AT1) subtype and prevents the blood pressure increasing effects of angiotensin II. Unlike angiotensin-converting enzyme (ACE) inhibitors, ARBs do not have the adverse effect of dry cough. Candesartan may be used to treat hypertension, isolated systolic hypertension, left ventricular hypertrophy and diabetic nephropathy. It may also be used as an alternative agent for the treatment of heart failure, systolic dysfunction, myocardial infarction and coronary artery disease. As with other drugs that inhibit the renin–angiotensin system, if candesartan is taken by pregnant women during the second or third trimester, it can cause injury and in some cases, death of the developing fetus. Symptomatic hypotension may occur in people who take candesartan and are volume-depleted or salt-depleted, as can also occur when diuretics are coadministered. Reduction in renal glomerular filtration rate may occur; people with renal artery stenosis may be at higher risk. Hyperkalemia may occur; people who are also taking spironolactone or eplerenone may be at higher risk. Anemia may occur, due to inhibition of the renin–angiotensin system. As with other angiotensin receptor blockers, candesartan can rarely cause severe liver injury.

* Carnitine is a quaternary ammonium compound involved in metabolism in most mammals, plants, and some bacteria. In support of energy metabolism, carnitine transports long-chain fatty acids into mitochondria to be oxidized for energy production, and also participates in removing products of metabolism from cells. Given its key metabolic roles, carnitine is concentrated in tissues like skeletal and cardiac muscle that metabolize fatty acids as an energy source. Healthy individuals, including strict vegetarians, synthesize enough L-carnitine in vivo to not require supplementation. Carnitine exists as one of two stereoisomers (the two enantiomers d-carnitine (S-(+)-) and l-carnitine (R-(-)-)). Both are biologically active, but only l-carnitine naturally occurs in animals, and d-carnitine is toxic as it inhibits the activity of the l-form. At room temperature, pure carnitine is a white powder, and a water-soluble zwitterion with low toxicity. Derived from amino acids, carnitine was first extracted from meat extracts in 1905, leading to its name from Latin, "caro/carnis" or flesh.

* Ceftaroline fosamil is a cephalosporin antibiotic with anti-MRSA activity. Ceftaroline fosamil is a prodrug of ceftaroline. It is active against methicillin-resistant Staphylococcus aureus (MRSA) and other Gram-positive bacteria. It retains some activity of later-generation cephalosporins having broad-spectrum activity against Gram-negative bacteria, but its effectiveness is relatively much weaker. It is currently being investigated for community-acquired pneumonia and complicated skin and skin structure infection. Uncomplicated SSSIs included "simple abscesses, impetiginous lesions, furuncles, and cellulitis." Complicated SSSIs included "infections either involving deeper soft tissue or requiring significant surgical intervention, such as infected ulcers, burns, and major abscesses or a significant underlying disease state that complicates the response to treatment." The FDA further noted that "superficial infections or abscesses in an anatomical site, such as the rectal area, where the risk of anaerobic or Gram-negative pathogen involvement is higher, [were also] considered complicated infections."The uncomplicated category (uSSSI) is most frequently caused by Staphylococcus aureus and Streptococcus pyogenes, whereas the complicated category (cSSSI) might also be caused by a number of other pathogens. The clinical studies indicated ceftaroline was well tolerated. The most common adverse reactions occurring in > 2% of subjects receiving ceftaroline in the pooled phase-III clinical trials were diarrhea, nausea, and rash. The warnings and precautions associated with ceftaroline include: Known serious hypersensitivity to ceftaroline or other members of the cephalosporin class. Anaphylaxis and anaphylactoid reactions. Clostridium difficile-associated diarrhea (CDAD) has been reported for nearly all antibacterial agents including ceftaroline, and may range in severity from mild diarrhea to fatal colitis. Prescribing ceftaroline in the absence of a proven or strongly suspected bacterial infection is unlikely to provide benefit to the patient and increases the risk of the development of drug-resistant bacteria. In the pooled phase-III CABP trials, 51/520 (9.8%) of subjects treated with ceftaroline compared to 24/534 (4.5%) of subjects treated with ceftriaxone seroconverted from a negative to a positive direct Coombs' test result. No clinical adverse reactions representing hemolytic anemia were reported in any treatment group. If anemia develops during or after treatment with ceftaroline, drug-induced hemolytic anemia should be considered. If drug-induced hemolytic anemia is suspected, discontinuation of ceftaroline should be considered and supportive care should be administered to the patient if clinically indicated. No clinical drug-drug interaction studies have been conducted with ceftaroline fosamil. In vitro studies in human liver microsomes indicated that neither ceftaroline fosamil nor ceftaroline inhibits the major cytochrome P450 isoenzymes. Therefore, neither ceftaroline fosamil nor ceftaroline is expected to inhibit or induce the clearance of drugs that are metabolized by these metabolic pathways in a clinically relevant manner. For pregnant or nursing mothers, ceftaroline fosamil should be used only if the potential benefit outweighs the potential risk to the fetus or child. Safety and effectiveness in pediatric children has not been studied. Because elderly people 65 years of age or older are more likely to have decreased renal function and ceftaroline is excreted primarily by the kidney, care should be taken in dose selection in this age group as in younger people with impaired renal function. Dosage adjustment is required in people with moderately (30 to ‰¤ 50 mL/min) or severely (< 30 mL/min) impaired renal function. The pharmacokinetics of ceftaroline in people with hepatic impairment have not been established. No adverse reactions occurred in greater than 5% of people receiving ceftaroline.

* Ceftolozane-Tazobactam is a combination antibiotic medication used for the treatment of complicated urinary tract infections and complicated intra-abdominal infections in adults. Ceftolozane is a  antibiotic, developed for the treatment of infections with gram-negative bacteria that are resistant to conventional antibiotics. It was studied for urinary tract infections, intra-abdominal infections and ventilator-associated bacterial pneumonia. The most common side effects include nausea (feeling sick), headache, constipation, diarrhea and fever. Ceftolozane is a type of antibiotic called a cephalosporin, which belongs to the wider group of antibiotics called beta-lactams. It works by interfering with the production of molecules that bacteria need to build their protective cell walls. This causes weakness in the bacterial cell walls which then become prone to collapse, ultimately leading to the death of the bacteria. Tazobactam blocks the action of bacterial enzymes called beta-lactamases. These enzymes enable bacteria to break down beta-lactam antibiotics like ceftolozane, making the bacteria resistant to the antibiotic's action. By blocking the action of these enzymes, tazobactam allows ceftolozane to act against bacteria that would otherwise be resistant to ceftolozane. Ceftolozane/tazobactam is indicated for the treatment of the following infections in adults caused by designated susceptible microorganisms: Complicated intra-abdominal infections; Acute pyelonephritis; Complicated urinary tract infections. Hospital-acquired bacterial pneumonia and Ventilator-associated bacterial pneumonia (HABP/VABP).

* Cilengitide (EMD 121974) is a molecule based on the cyclic peptide cyclo(-RGDfV-), which is selective for alphav integrins, which are important in angiogenesis (forming new blood vessels), and other aspects of tumor biology. Hence, it is under investigation for the treatment of glioblastoma, where it may act by inhibiting angiogenesis, and influencing tumor invasion and proliferation. The European Medicines Agency has granted cilengitide orphan drug status. Cilengitide seems to function by inhibiting the FAK/src/AKT pathway and inducing apoptosis in endothelial cells. Preclinical studies in mice of cilengitide were able to demonstrate efficacious tumor regression. In a rat xenograft model, cilengitide was able to potentiate the cytotoxic effects of radiation when cilengitide was administered prior to radiation therapy. When combined with radiation, inhibition of integrin expression by cilengitide synergistically improves the cytotoxic effects of ionizing radiation for glioblastoma. Phase II studies were able to demonstrate that cilengitide as a potential monotherapy in patients with recurrent glioblastoma with high intratumor drug levels when 2000 mg of cilengitide is given twice weekly. Cilengitide is well tolerated, in combination with radiation and temozolomide, at a dose of 2000 mg in patients with newly diagnosed glioblastoma, regardless of MGMT promoter status. In a phase I/IIa study, the addition of cilengitide to the standard of care for newly diagnosed glioblastoma (surgical resection followed by temozolomide and radiation therapy) improves progression-free survival and overall survival in patients with MGMT promoter methylation.

* Colloidal Silver. Silver(1+) is a silver cation, a monovalent inorganic cation, a monoatomic monocation and an elemental silver. The medical uses of silver include its use in wound dressings, creams, and as an antibiotic coating on medical devices. Wound dressings containing silver sulfadiazine or silver nanomaterials may be used to treat external infections. The limited evidence available shows that silver coatings on endotracheal breathing tubes may reduce the incidence of ventilator-associated pneumonia. There is tentative evidence that using silver-alloy indwelling catheters for short-term catheterizing will reduce the risk of catheter-acquired urinary tract infections. Indicated for  Dental Pulp Necrosis (Phase 4); Diabetic Foot (Phase 4); Foot Ulcer (Phase 4); Pain, Postoperative (Phase 4); Skin Ulcer; Ulcer (Phase 4.); Sinusitis (Phase 2) Hernia (Phase 1); Hernia, Abdominal (Phase 1); Hernia, Ventral (Phase 1); Incisional Hernia (Phase 1); Chronic Disease (Phase 1).

* Compound-44 is a tricyclic peptide PCSK9 inhibitor. Proprotein convertase subtilisin-like/kexin type 9 (PCSK9) is a key regulator of plasma LDL-cholesterol (LDL-C) and a clinically validated target for the treatment of hypercholesterolemia and coronary artery disease. This molecule represents the first report of highly potent and orally bioavailable macrocyclic peptide PCSK9 inhibitor with an overall favorable profile as a once-daily oral lipid-lowering agent. The clearance of the molecule has been shifted over time in the drug discovery campaign from predominantly hepatic to renal by reducing OATP 1B1 transporter activity.

* CTIBD or 4-(4-(4-chlorophenyl)-3-(trifluoromethyl)isoxazol-5-yl)benzene-1,3-diol and its derivatives are novel chemical activators of the bladder BKCa channel and potential candidates for OAB therapeutics. CTIBD directly activates the BKCa channel and relaxes urinary bladder smooth muscle of rats. In an acetic acid-induced overactive bladder (OAB) model, intraperitoneal injection of 20 mg/kg CTIBD effectively restored frequent voiding contraction and lowered voiding volume without affecting other bladder function parameters. CTIBD concentration-dependently reduced acetylcholine-induced contraction of urinary bladder smooth muscle strips. CTIBD altered the gating kinetics of the channel by dramatically slowing channel closing without effecting channel opening. When CTIBD was applied to the treated extracellular side of the channel, the conductance-voltage relationship of the channel shifted toward a negative value, and the maximum conductance increased in a concentration-dependent manner. The large-conductance calcium-activated potassium channel (BKCa channel) is expressed on various tissues and is involved in smooth muscle relaxation. The channel is highly expressed on urinary bladder smooth muscle cells and regulates the repolarization phase of the spontaneous action potentials that control muscle contraction.

* Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver. Insulin is a peptide hormone produced by beta cells of the pancreatic islets; it is considered to be the main anabolic hormone of the body. It regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of glucose from the blood into liver, fat and skeletal muscle cells. In these tissues the absorbed glucose is converted into either glycogen via glycogenesis or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both. Glucose production and secretion by the liver is strongly inhibited by high concentrations of insulin in the blood. Circulating insulin also affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve body fat. Beta cells are sensitive to blood sugar levels so that they secrete insulin into the blood in response to high level of glucose; and inhibit secretion of insulin when glucose levels are low. Insulin enhances glucose uptake and metabolism in the cells, thereby reducing blood sugar level. Their neighboring alpha cells, by taking their cues from the beta cells, secrete glucagon into the blood in the opposite manner: increased secretion when blood glucose is low, and decreased secretion when glucose concentrations are high. Glucagon increases blood glucose level by stimulating glycogenolysis and gluconeogenesis in the liver. The secretion of insulin and glucagon into the blood in response to the blood glucose concentration is the primary mechanism of glucose homeostasis. Decreased or absent insulin activity results in diabetes mellitus, a condition of high blood sugar level (hyperglycaemia). There are two types of the disease. In diabetes mellitus type 1, the beta cells are destroyed by an autoimmune reaction so that insulin can no longer be synthesized or be secreted into the blood. In diabetes mellitus type 2, the destruction of beta cells is less pronounced than in type 1, and is not due to an autoimmune process. Instead, there is an accumulation of amyloid in the pancreatic islets, which likely disrupts their anatomy and physiology. The pathogenesis of type 2 diabetes is not well understood but reduced population of islet beta-cells, reduced secretory function of islet beta-cells that survive, and peripheral tissue insulin resistance are known to be involved. Type 2 diabetes is characterized by increased glucagon secretion which is unaffected by, and unresponsive to the concentration of blood glucose. But insulin is still secreted into the blood in response to the blood glucose. As a result, glucose accumulates in the blood.

* Montbretin A is a new anti-diabetic compound derived from a garden flower approved by Health Canada for Phase 1 human trials. Montbretin A slows down the degradation of the starch component in food, but does not affect the simple sugars. Montbretin A (MbA) works by inhibiting the enzyme alpha-amylase. When MbA inhibits the alpha-amylase enzyme, starch doesn't break down immediately and instead travels down into the lower gut. Normally, the alpha-amylase enzyme breaks down starch from foods such as rice and bread into complex sugars called oligosaccharides. Oligosaccharides are then further degraded by alpha-glucosidase enzymes in the gut wall, releasing glucose into the bloodstream, which causes blood sugar levels to spike in Type 2 diabetics. Current drugs that target the same enzyme system usually inhibit the alpha-glucosidase enzyme, stopping the oligosaccharides or complex sugars from being broken down, and preventing the release of glucose. The downside of these drugs is that the oligosaccharides that are shunted down provide 'fast food' for the gut bacteria further down, and these gut bacteria produce a lot of gas as a side product…so the patient tends to suffer from diarrhea and flatulence. Since MbA prevents starch from being broken down into oligosaccharides, the full starch polymer will make its way into the lower gut. The bacteria down there can degrade that, although more slowly.  Animal studies on diabetic rats showed that MbA controlled blood sugar levels efficiently.

* Nemonoxacin is a non-fluorinated quinolone antibiotic undergoing clinical trials. It has the same mechanism of action as fluouroquinolones; it inhibits DNA gyrase, preventing DNA synthesis, gene duplication, and cell division. The U.S. Food and Drug Administration (FDA) has granted nemonoxacin qualified infectious disease product (QIDP) and fast track designations for community-acquired bacterial pneumonia (CAP) and acute bacterial skin and skin-structure infections (ABSSSI). Nemonoxacin has a broad spectrum of activity against Gram-positive, Gram-negative, and atypical pathogens, including activity against methicillin-resistant Staphylococcus aureus (MRSA) (MIC90 1 g/ml) and vancomycin-resistant pathogens. However, it was less active against Gram-negative pathogens such as Escherichia coli, Proteus mirabilis, and Pseudomonas aeruginosa, with MIC90 values of 32, 16, and 32 g/ml, respectively. The new drug also is effective against C.difficile isolates that are resistant to other quinolones, and is more potent than levofloxacin or moxifloxacin.

* Nifedipine is a calcium channel blocker medication used to manage angina, high blood pressure, Raynaud's phenomenon, and premature labor. It is one of the treatments of choice for Prinzmetal angina. It may be used to treat severe high blood pressure in pregnancy. Its use in preterm labor may allow more time for steroids to improve the baby's lung function and provide time for transfer of the mother to a well qualified medical facility before delivery. It is a calcium channel blocker of the dihydropyridine type. Nifedipine is taken by mouth and comes in fast- and slow-release formulations. Common side effects include lightheadedness, headache, feeling tired, leg swelling, cough, and shortness of breath. Serious side effects may include low blood pressure and heart failure. There is tentative evidence that its use in pregnancy is safe; however, it is not recommended during breastfeeding. The approved uses are for the long-term treatment of hypertension and angina pectoris. In hypertension, recent clinical guidelines generally favour diuretics and ACE inhibitors, although calcium channel antagonists, along with thiazide diuretics, are still favoured as primary treatment for patients over 55 and black patients. Nifedipine has been used frequently as a tocolytic (agent that delays premature labor). A Cochrane review has concluded that it has benefits over placebo or no treatment for prolongation of pregnancy. It also has benefits over beta-agonists and may also have some benefits over atosiban and magnesium sulfate, although atosiban results in fewer maternal adverse effects. No difference was found in the rate of deaths among babies around the time of birth, while data on longer-term outcomes is lacking. Raynaud's phenomenon is often treated with nifedipine. A 2005 meta-analysis showed modest benefits (33% decrease in attack severity, 2.8-5 reduction in absolute number of attacks per week); it does conclude that most included studies used low doses of nifedipine. Topical nifedipine has been shown to be as effective as topical nitrates for anal fissures. Nifedipine is also used in high-altitude medicine to treat high altitude pulmonary edema. Nifedipine is one of the main choices for the treatment of Prinzmetal angina due to its vasodilating effects on the coronary arteries. Other uses include painful spasms of the esophagus such as from cancer or tetanus. It is also used for the small subset of people with pulmonary hypertension.Finally, nifedipine can be used in the treatment of renal calculi, which are commonly referred to as kidney stones. Studies have indicated that it helps to relieve renal colic. However, alpha blockers (such as tamsulosin) have been described as being significantly better. Nifedipine treats chilblains by helping to dilate blood vessels and improve circulation. Side effects can include flushing of the face and neck, nausea, dizziness, and swelling in the hands or feet. Nifedipine rapidly lowers blood pressure, and patients are commonly warned they may feel dizzy or faint after taking the first few doses. Tachycardia (fast heart rate) may occur as a reaction. Patients are warned not to consume anything containing grapefruit or grapefruit juice, as they raise blood nifedipine levels. There are several possible mechanisms, including the inhibition of CYP3A4-mediated metabolism. As calcium channel blocker, nifedipine has a risk of causing gingival hyperplasia. Nifedipine is a calcium channel blocker. Although nifedipine and other dihydropyridines are commonly regarded as specific to the L-type calcium channel, they also possess nonspecific activity towards other voltage-dependent calcium channels. Nifedipine has additionally been found to act as an antagonist of the mineralocorticoid receptor, or as an antimineralocorticoid.

* Pexiganan is a polypeptide antibiotic agent derivative of Magainin. Pexiganan is a microbicide and antiinfective agent  with potent and broad-spectrum antimicrobial with low toxicity against mammalian cells. It is being developed as a topical therapy for infected foot ulcers in patients with diabetes. Pexiganan is a 22-amino-acid antimicrobial peptide derived from magainin peptides isolated from the skin of the African clawed frog. It demonstrates antimicrobial activity against a broad range of organisms, including gram-positive aerobes and anaerobes, such as staphylococcus, streptococcus, enterococcus, corynebacterium, pseudomonas, acinetobacter, strenotrophomonas, bacteroides, and other species. Phase III clinical studies proved pexiganan to be efficient in wound healing, with few reports of toxicity.

* PIEZO2 Factor or Piezo-type mechanosensitive ion channel component 2 is a protein that in humans is encoded by the PIEZO2 gene. The PIEZO2 protein has a role in rapidly adapting mechanically activated (MA) currents in somatosensory neurons. PIEZO2 is typically found in tissues that respond to physical touch, such as Merkel cells, and is thought to regulate light touch response. PIEZO2, may be responsible for the powerful urge to urinate that we normally feel several times a day. This gene helps at least two different types of cells in the body sense when our bladders are full and need to be emptied. Gain-of-function mutations in the mechanically activated ion channel PIEZO2 cause a subtype of Distal Arthrogryposis. Mice without PIEZO2 in their proprioceptive neurons show uncoordinated body movements, indicating that PIEZO2 plays a role in mammalian proprioception. PIEZO2 mutations link Gordon syndrome (distal arthrogryposis type 3), Marden-Walker syndrome and Arthrogryposis (Distal Arthrogryposis Type 5).

* Reldesemtiv (CK-2127107) is an activator of skeletal muscle troponin, a calcium-sensitive sarcomere protein. By slowing the rate of calcium release in skeletal muscles, it improves their contractility. Several trials realized in healthy volunteers against placebo have showed its good tolerance and its effectiveness on muscle strength; it is being studied as a potential treatment for diseases associated with fatigue or muscle weakness. Developed by Cytokinetics, reldesemtiv was evaluated between December 2015 and May 2018 in 18 centers in North America in 70 patients with type II, III and IV SMA, over 12 years-old. For two months, participants in this phase II, randomized, double-blind trial received orally either reldesemtiv twice daily at a dose of 150 mg (24 participants) or 450 mg (20 participants), or placebo (26 participants). The results, published in February 2021, show:  good tolerance to the two doses tested, a significant improvement in respiratory function (maximum expiratory pressure or MEP) in patients on reldesemtiv at both doses, compared to the placebo group, a significant increase in the walking distance covered in six minutes by the patients who received reldesemtiv 450 mg compared to the placebo group. The investigators of this trial suggest to evaluate this treatment, which does not affect the production of SNM like the drugs recently authorized in SMA, in a larger number of patients. Despite the recent approvals of edaravone for the treatment of amyotrophic lateral sclerosis (ALS) and nusinersen for the treatment of spinal muscle atrophy (SMA), therapeutic options remain limited and represent a significant medical need. The discovery of reldesemtiv, a second-generation fast skeletal muscle troponin activator (FSTA) that increases force production at submaximal stimulation frequencies, is reported. Property-based optimization of high throughput screening hit 1 led to compounds with improved free exposure and in vivo muscle activation potency compared to the first-generation FSTA, tirasemtiv. Reldesemtiv demonstrated increased muscle force generation in a phase 1 clinical trial and is currently being evaluated in clinical trials for the treatment of amyotrophic lateral sclerosis.

* Salvigenin is a natural polyphenolic compound, with neuroprotective effect. Salvigenin, a potent human monoamine oxidase-A -hMAO-A isoform inhibitor, has antitumor cytotoxic and immunomodulatory properties. Salvigenin has dose-dependent analgesic effect so that it can be useful in controlling of inflammations, acute and chronic pain. Salvigenin has been found to have cytotoxic effects on various forms of cancer cells, such as colon adenocarcinoma, breast adenocarcinoma and glioblastoma. Further salvigenin has beneficial potential in the medicine for the treatment of diabetes and protects cells against oxidative stress.

* Solabegron is a drug which acts as a selective agonist for the beta3 adrenergic receptor. It is being developed for the treatment of overactive bladder and irritable bowel syndrome. It has been shown to produce visceral analgesia by releasing somatostatin from adipocytes. Solabegron relaxes the bladder smooth muscle by stimulating beta3 adrenoceptors, a novel mechanism compared with older established drug treatments for overactive bladder syndrome such as the anticholinergic agents. Astellas Pharma has developed the first commercially available beta3 adrenergic receptor, mirabegron, which is now licensed in Japan and the U.S. exclusively for treatment of overactive bladder syndrome. A Phase II study of solabegron for overactive bladder (OAB) looked at 258 patients with moderate-to-severe incontinence experiencing an average of 4.5 wet episodes per day. Results demonstrated a statistically significant improvement with solabegron as compared with placebo, as measured by the percentage reduction of the number of wet episodes and the absolute number of daily voids. A Phase II study for irritable bowel syndrome (IBS) evaluated 102 patients with IBS. Solabegron demonstrated significant reduction in pain associated with the disorder and a trend for greater improvement in the quality of life, when compared with a placebo. Both Phase II studies indicated a tolerability profile for Solabegron that was similar to placebo. The OAB patients did not suffer from dry mouth, constipation, increase in heart rate or cognitive issues. This drug does not bind to acetylcholine receptors so side effects are expected to be minor.

* Solifenacin is a medicine used to treat overactive bladder and neurogenic detrusor overactivity (NDO). It may help with incontinence, urinary frequency, and urinary urgency. Benefits appear similar to other medications in the class. Common side effects include dry mouth, constipation, and urinary tract infection. Severe side effects may include urinary retention, QT prolongation, hallucinations, glaucoma, and anaphylaxis. It is unclear if use is safe during pregnancy. It is of the antimuscarinic class and works by decreasing bladder contractions. It is used to treat overactive bladder. It may help with incontinence, urinary frequency, and urinary urgency. Benefits appear similar to other antimuscarinics such as oxybutynin, tolterodine, and darifenacin. It is also used to treat neurogenic detrusor overactivity (NDO), a form of bladder dysfunction related to neurological impairment, in children ages two years and older. NDO is a dysfunction of the bladder that results from disease or injury in the nervous system. With NDO, there is overactivity of the bladder wall muscle, which normally relaxes to allow storage of urine. The bladder wall muscle overactivity results in sporadic bladder muscle contraction, which increases pressure in the bladder and decreases the volume of urine the bladder can hold. If NDO is not treated, increased pressure in the bladder can put the upper urinary tract at risk of harm, including possible permanent damage to the kidneys. In addition, spontaneous bladder muscle contractions can lead to unexpected and frequent leakage of urine with symptoms of urinary urgency (immediate urge to urinate), frequency (urinating more often than normal) and incontinence (loss of bladder control). Solifenacin is contraindicated for people with urinary retention, gastric retention, uncontrolled or poorly controlled closed-angle glaucoma, severe liver disease (Child-Pugh class C)] and hemodialysis. Long QT syndrome is not a contraindication although solifenacin, like tolterodine and darifenacin, binds to hERG channels of the heart and may prolong the QT interval. This mechanism appears to be seldom clinically relevant. The most common side effects of solifenacin are dry mouth, constipation and urinary tract infection. As all anticholinergics, solifenacin may rarely cause hyperthermia due to decreased perspiration. Somnolence (sleepiness or drowsiness) has been reported. Severe allergic reactions, such as angioedema (swelling beneath the skin) and anaphylaxis, have been reported in people treated with solifenacin succinate and may be life-threatening. Solifenacin is metabolized in the liver by the cytochrome P450 enzyme CYP3A4. When administered concomitantly with drugs that inhibit CYP3A4, such as ketoconazole, the metabolism of solifenacin is impaired, leading to an increase in its concentration in the body and a reduction in its excretion. As stated above, solifenacin may also prolong the QT interval. Therefore, administering it concomitantly with drugs which also have this effect, such as moxifloxacin or pimozide, can theoretically increase the risk of arrhythmia. Solifenacin is a competitive cholinergic receptor antagonist, selective for the M3 receptor subtype. The binding of acetylcholine to these receptors, particularly M3, plays a critical role in the contraction of smooth muscle. By preventing the binding of acetylcholine to these receptors, solifenacin reduces smooth muscle tone in the bladder, allowing the bladder to retain larger volumes of urine and reducing the number of micturition, urgency and incontinence episodes. Because of a long elimination half life, a once-a-day dose can offer 24-hour control of the urinary bladder smooth muscle tone.

* Tamsulosin is a medication used to treat symptomatic benign prostatic hyperplasia (BPH) and chronic prostatitis and to help with the passage of kidney stones. The evidence for benefit with a kidney stone is better when the stone is larger. Common side effects include dizziness, headache, sleeplessness, nausea, blurry vision, and sexual problems. Other side effects may include feeling lightheaded with standing and angioedema. Tamsulosin is an alpha blocker and works by relaxing muscles in the prostate. Specifically it is an alpga1 adrenergic receptor blocker. Tamsulosin is primarily used for benign prostatic hyperplasia and to help with the passage of kidney stones. Tamsulosin, however, appears to be effective only for stones over 4 mm and less than 10 mm in size. Tamsulosin is also used as an add-on treatment for acute urinary retention. People may void more successfully after catheter removal if they are taking tamsulosin. People taking tamsulosin also are less likely to need re-catheterization. Tamsulosin does not decrease the overall size of the prostate in men with BPH, and is not recommended for prevention of prostate cancer.

* Tozinameran is an mRNA encoding full length of spike protein analog of SARS-CoV-2. Target severe acute respiratory syndrome coronavirus 2 spike glycoprotein. Coronavirus disease – COVID-19. Active immunization (SARS-CoV-2). The vaccination requires two primary series doses given three weeks apart. A third primary series dose may be administered at least 4 weeks after the second dose to individuals who are determined to have certain kinds of immunocompromise. A single booster dose of the vaccine may be administered at least 6 months after completion of a primary series with Tozinameran or with a different authorized COVID-19 vaccine.

* Trichloroacetic acid (TCA) is an analogue of acetic acid. It is a well-known caustic agent extensively used in dermatology, mainly in cosmetic peelings. It causes coagulative necrosis of cells through wide protein denaturation and resultant structural cell death. It is also used for ingrown toenails where TCA offers extra advantages, including coagulation and potent local anesthetic effects. TCA is a strong acid. It is widely recognized that skin contact of TCA has the potential to produce acid burns, and ingestion of TCA has the potential to damage tissues of the gastrointestinal tract or produce systemic acidosis, even though specific studies of these effects do not appear in the literature. TCA is relatively nontoxic to humans under circumstances of low exposures such as those encountered in chlorinated drinking water. In addition, the mode of tumor induction – peroxisomal proliferation – in animals is not relevant for humans.

* Turmeric-Mix. Turmeric, a plant in the ginger family, is native to Southeast Asia and is grown commercially in that region, primarily in India. Its rhizome (underground stem) is used as a culinary spice and traditional medicine. Historically, turmeric was used in Ayurveda and other traditional Indian medical systems, as well as Eastern Asian medical systems such as traditional Chinese medicine. In India, it was traditionally used for disorders of the skin, upper respiratory tract, joints, and digestive system. Today, turmeric is promoted as a dietary supplement for a variety of conditions, including arthritis, digestive disorders, respiratory infections, allergies, liver disease, depression, high blood cholesterol, osteoarthritis pain, itching caused by chronic kidney disease, prediabetes, tuberculosis, Alzheimer's disease, cancer, inflammatory bowel diseases, and lowering the risk of a heart attack after bypass surgery. Turmeric is a common spice and a major ingredient in curry powder. Curcumin is a major component of turmeric, and the activities of turmeric are commonly attributed to curcuminoids (curcumin and closely related substances). Curcumin gives turmeric its yellow color. Turmeric dietary supplements are made from the dried rhizome and typically contain a mixture of curcuminoids. Turmeric is also made into a paste for skin conditions. Turmeric supplements may boost the immune system before Covid-19 vaccination. The recording plays the sound frequencies of Curcumin, Desmethoxycurcumin, Bisdemethoxycurcumin, Germacrone and Zingiberene.