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Ethacrynic acid is a "water pill" (diuretic) that works in your kidneys to increase the amount of urine you make. This helps your body get rid of extra water. This medication is used to decrease swelling (edema) caused by conditions such as cancer, congestive heart failure, liver disease, and kidney disease. This effect can help your kidneys work better and lessen symptoms such as trouble breathing and swelling in your ankles, feet, hands, or belly.Ethacrynic acid powder

This medication should not be used for infants.

How to use Ethacrynic Acid

Take this medication by mouth as directed by your doctor, usually once or twice a day after a meal. If you take this drug too close to bedtime, you may need to wake up to urinate. It is best to take this medication at least 4 hours before your bedtime. Consult your doctor or pharmacist if you have questions about your dosing schedule.

The dosage is based on your medical condition and response to treatment. To reduce your risk of side effects, your doctor may direct you to start this medication at a low dose and gradually increase your dose. Your doctor will adjust your dose based on your medical condition, response to treatment, and lab tests (such as sodium, potassium, chloride levels). Some people may be directed to take this medication every other day or only when needed. Follow your doctor's directions carefully.

If your doctor has directed you to take this medication on a regular schedule, take it regularly to get the most benefit from it. To help you remember, take it at the same time(s) each day.
Learn how to convert milligrams (mg) to milliliters (ml) with this article and Let's say we want to work out how many ml there are in 45mg of it. It is also equal to 1 cubic centimeter, or about 15 minims. Milligrams and Milliliters are commonly used measurement units used around the world. Any unit of. ligands endoxifen and cyclofenil-endoxifen hybrids covalently linked to the ERβ is expressed in many tissues and is the predominant ER in required incubation period, cells were fixed in 1 mL ethanol and µL PBS .. mmol) was reacted with endoxifen derivative (1 eq., mg, mmol).Cyclofenil powder

found in urine and authors did not report any analytical figure of merit to the active principle ( mg per tablet) was purchased in local drugstores. to- charge ratio equals Da) followed by the formation of a second even mL min Cyclofenil originally presents weak fluorescence in solution and it was not detected. Certain advertising, labelling and packaging requirements may also be a consequence of millilitres or less. Basil oil CYCLOFENIL. Many approaches have been investigated to improve the selectivity of drugs The high affinity nonsteroidal ER ligand cyclofenil diphenol (F) [32,33] .. After the required incubation period, cells were fixed in 1 mL ethanol and .. mg, mmol) was reacted with endoxifen derivative (1 eq., mg, mmol).

(b) that contain more than % by weight of any substance having the . “mg” for milligram; and. “ml” for millilitre; and .. Croton Seed. Curare. Cyclofenil supplied is labelled to show a maximum dose of mg and a maximum . medicinal product is equivalent to % of hydrocortisone, calculated in. cyclofenil suggested similarity in their effectiveness. Side effects natives to breastfeeding exist may seek lactation suppression on personal or Oral bromocriptine mg twice daily for 14 days (n = 49) versus oral pyridoxine Therefore, mL of breast secretion was manually collected from each woman daily.
Bisoprolol fumarate and hydrochlorothiazide tablets are indicated for the treatment of hypertension. It combines two antihypertensive agents in a once-daily dosage: a synthetic beta1-selective (cardioselective) adrenoceptor blocking agent (bisoprolol fumarate) and a benzothiadiazine diuretic (hydrochlorothiazide).

Bisoprolol fumarate is chemically described as (±)-1-[4-[[2-(1-methylethoxy)ethoxy]methyl]phenoxy]-3-[(1-methylethyl)amino ]-2-propanol(E)-2-butenedioate (2:1) (salt). It possesses an asymmetric carbon atom in its structure and is provided as a racemic mixture. The S(-) enantiomer is responsible for most of the beta-blocking activity. Its empirical formula is (C18H31NO4)2•C4H4O4 and it has a molecular weight of 766.97. Its structural formula is:Bisoprolol powder

Bisoprolol fumarate is a white crystalline powder, approximately equally hydrophilic and lipophilic, and readily soluble in water, methanol, ethanol, and chloroform.

Hydrochlorothiazide (HCTZ) is 6-Chloro-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. It is a white, or practically white, practically odorless crystalline powder. It is slightly soluble in water, sparingly soluble in dilute sodium hydroxide solution, freely soluble in n-butylamine and dimethylformamide, sparingly soluble in methanol, and insoluble in ether, chloroform, and dilute mineral acids. Its empirical formula is C7H8ClN3O4S2 and it has a molecular weight of 297.73. Its structural formula is:
Inactive ingredients include Corn Starch, Dibasic Calcium Phosphate, Hypromellose, Magnesium Stearate, Microcrystalline Cellulose, Polyethylene Glycol, Polysorbate 80, and Titanium Dioxide. The 10 mg/6.25mg tablet also contains Colloidal Silicon Dioxide. The 5 mg/6.25 mg tablet also contains Colloidal Silicon Dioxide, and Red and Yellow Iron Oxide. The 2.5 mg/6.25 mg tablet also contains Crospovidone, Pregelatinized Starch, and Yellow Iron Oxide.

Bisoprolol fumarate and HCTZ have been used individually and in combination for the treatment of hypertension. The antihypertensive effects of these agents are additive; HCTZ 6.25 mg significantly increases the antihypertensive effect of bisoprolol fumarate. The incidence of hypokalemia with the bisoprolol fumarate and HCTZ 6.25 mg combination (B/H) is significantly lower than with HCTZ 25 mg. In clinical trials of bisoprolol fumarate and hydrochlorothiazide tablets, mean changes in serum potassium for patients treated with bisoprolol fumarate and hydrochlorothiazide tablets 2.5/6.25 mg, 5/6.25 mg or 10/6.25 mg or placebo were less than ± 0.1 mEq/L. Mean changes in serum potassium for patients treated with any dose of bisoprolol in combination with HCTZ 25 mg ranged from -0.1 to -0.3 mEq/L.

Bisoprolol fumarate is a beta1-selective (cardioselective) adrenoceptor blocking agent without significant membrane stabilizing or intrinsic sympathomimetic activities in its therapeutic dose range. At higher doses (≥ 20 mg) bisoprolol fumarate also inhibits beta2-adrenoreceptors located in bronchial and vascular musculature. To retain relative selectivity, it is important to use the lowest effective dose.

Hydrochlorothiazide is a benzothiadiazine diuretic. Thiazides affect renal tubular mechanisms of electrolyte reabsorption and increase excretion of sodium and chloride in approximately equivalent amounts. Natriuresis causes a secondary loss of potassium.
Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression, and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels are not available. Using controlled-cortical impact as an experimental model of brain trauma in adult mice, we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on the appearance of depressive-like behavior. We demonstrate that this alteration in behavior is associated with an impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in the expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission from hyperpolarizing to depolarizing after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.Bumetanide powder

Introduction
Brain trauma is the main cause of disability all over the world with a very high prevalence in developed countries (Meyer et al., 2008; Bondi et al., 2015). According to the World Health Organization and the Centers for Disease Control and Prevention (Meyer et al., 2008), brain trauma classification is based on multiple factors such as altered neurological functions, brain area of interest and genetic variations. Altogether, these factors lead to highly individualized injuries. Sequels of trauma include low prevalence post-traumatic epilepsies (PTEs), with a severity and occurrence dependent on trauma severity (Kelly et al., 2015; Bragin et al., 2016), and cognitive dysfunctions and depression-like phenotypes are also commonly associated (Peeters et al., 2015; Perry et al., 2015; Stein et al., 2015). Following brain trauma, neuronal cell death occurs and more particularly within the neurons of the dentate gyrus of the hippocampus (Ren et al., 2015; Samuels et al., 2015), leading to hippocampal volume reduction (Samuels et al., 2015; Anacker and Hen, 2017). These observations could be related to changes in post-traumatic neurogenesis in the hippocampus. This has been proposed to be a useful marker of therapeutic treatment efficacy (Brandon and McKay, 2015; Alvarez et al., 2016).

In a wide range of neurological and psychiatric disorders, GABAergic signaling is affected through chloride homeostasis impairment triggered by a down regulation of the main neuronal-specific chloride and potassium extruder, KCC2, and up regulation of the chloride importer NKCC1, respectively (Medina et al., 2014). Similar changes in GABAergic transmission have been reported in a different model of brain trauma (Ben-Ari, 2017). This leads to depolarization and also an excitatory action of GABA that could perturb the generation of behaviorally relevant oscillations and integrative properties of brain networks (Rivera et al., 1999; Luscher et al., 2011; Kahle et al., 2013; Medina et al., 2014; Ben-Ari, 2017). These shifts have been observed notably in developmental disorders including autism spectrum disorders (ASDs) (Tyzio et al., 2014), stroke (Jaenisch et al., 2010; Xu et al., 2016) and epilepsy (Pallud et al., 2014; Tyzio et al., 2014; Kelley et al., 2016). The interaction between major depressive disorders (MDDs) and GABAergic neurotransmission has been suggested in a genetic mice model of GABA(B)-R knock-out (Mombereau et al., 2005) and in studies showing an antidepressant effect of potent and selective blockage of GABA(A) transmission (Rudolph and Knoflach, 2011) at both the hippocampus (Boldrini et al., 2013) and mesolimbic system (Kandratavicius et al., 2014). In addition, several observations link chloride homeostasis to secondary neurogenesis through GABA(A) neurotransmission (Luscher et al., 2011; Ostroumov et al., 2016). The generation of new neurons within the DG requires different steps: first, the transition from quiescent to proliferative progenitors, then their differentiation to immature neurons in a GABAergic-dependent manner (Chell and Frisén, 2012; Moss and Toni, 2013). In that context, it’s well-accepted that brain trauma alters neurogenesis (Perry et al., 2015; Stein et al., 2015). In the past decade, the relationship between GABA neurotransmission and neurogenesis has been well-established. Ge and collaborators have shown that GABA receptors are expressed in the progenitor cells and that GABA itself, either ambient or synaptically-released GABA, could act at different steps during neurogenesis from proliferation to cell differentiation and finally synaptic integration (Ge et al., 2006; Anacker and Hen, 2017). In addition, the GABAergic polarity acts on the cell integration (Ge et al., 2006) but also in cell proliferation (Sun et al., 2012), thus establishing a causal link between cell cycling and cell cycle exit on depolarizing GABA condition (Scharfman and Bernstein, 2015; Hu J.J. et al., 2017). Apart from the monoamine hypothesis, a new theory based on the GABA release itself has been proposed to contribute to depression. GABA release has been demonstrated to be impaired in psychiatric disorders and particularly in depression (Luscher et al., 2011; Gabbay et al., 2012). More particularly, the GABAergic receptors have been shown to be decreased in expression and function in the dentate gyrus of depressed patients (Luscher et al., 2011; Lüscher and Fuchs, 2015) and brain tissues collected from suicide patients with a history of depression and anxiety (Merali et al., 2004). One of the first phenomenon linking depression and the hippocampus is the change in hippocampal volume observed both in rodent and in human (Savitz et al., 2010; Schuhmacher et al., 2013; Roddy et al., 2018). This is a common trait observed when the hypothalamic–pituitary–adrenal (HPA) axis is impaired. Other brain regions such as cingulate cortex, prefrontal cortex or even amygdala are also associated with depression (Drevets et al., 2008). In addition to volume changes other functions are changed in the hippocampus of animal displaying DLB, e.g., modified volume (Roddy et al., 2018), impaired GABAergic function (Merali et al., 2004), increase in excitability and monoamine dysfunction (Samuels et al., 2015) as well as impaired secondary neurogenesis and cognitive deficit (Ferguson et al., 2016; Anacker and Hen, 2017). Taken together, this makes the hippocampal formation a important and valuable structure to study depression in TBI models.

Parvalbumin-containing interneurons are the principal source of GABA release within the dentate gyrus and thus potential candidates to explain controlled-cortical impact (CCI)-induced dysregulations through their role in the synchronicity of hippocampal networks (Curia et al., 2008; Drexel et al., 2011; Shiri et al., 2014). Moreover, it is accepted that the activity of this class of interneurons could act on secondary neurogenesis by providing a source of ambient GABA (Song et al., 2012; Butler et al., 2016; Hu D. et al., 2017; Pérez-Domínguez et al., 2017), but little is known about the relationship that exists between parvalbumin-containing interneurons and the establishment of post-traumatic depression (Earnheart et al., 2007; Luscher et al., 2011; Fenton, 2015). Moreover, in human depression, their action is far from being established (Khundakar et al., 2011; Pehrson and Sanchez, 2015; Smiley et al., 2016).

Interestingly, the NKCC1 chloride importer antagonist bumetanide has been shown to attenuate many disorders like ASD, Parkinson’s disease, and schizophrenia as well as some CCI-induced consequences. This stresses the therapeutic potential of restoring low (Cl-)i levels and an efficient GABAergic inhibition (Lemonnier et al., 2013, 2016; Damier et al., 2016; Xu et al., 2016; Ben-Ari, 2017). Although, it has been previously shown that bumetanide could have various positive effects on TBI models (Hui et al., 2016; Zhang et al., 2017) and could also act on secondary neurogenesis in stroke condition (Xu et al., 2016), yet nothing is known about the early action of this compound prior to the establishment of depressive-like behaviors (DLB). Our results showed that brain trauma disrupts chloride homeostasis, leading to hippocampal network disturbances and impaired neurogenesis associated with DLB. Early restoration of chloride homeostasis, using the NKCC1 inhibitor bumetanide rapidly after trauma, attenuates the severity of post-traumatic alterations notably by reducing interneuron loss. This, taken together, suggests a therapeutic potential of this FDA-approved compound after trauma.
Carteolol hydrochloride is a beta-adrenergic antagonist used as an anti-arrhythmia agent, an anti-angina agent, an antihypertensive agent, and an antiglaucoma agent. Carteolol Hydrochloride is a nonselective beta-adrenoceptor blocking agent for beta-1 and beta-2 receptors with no membrane-stabilizing activity but moderate intrinsic sympathomimetic effects.Carteolol powder
References 1: Chikama T, Araie M, Nishida T. [Influence on ocular surface and intraocular pressure of switching from preservative-containing to preservative-free carteolol hydrochloride ophthalmic solution]. Nippon Ganka Gakkai Zasshi. 2013 May;117(5):419-26. Japanese. PubMed PMID: 23855234. 2: Yao Q, Yu X, Zheng T, Liu H, Yang Y, Yi P. Spectroscopic studies on the interaction of carteolol hydrochloride and urea-induced bovine serum albumin. Spectrochim Acta A Mol Biomol Spectrosc. 2013 Sep;113:447-51. doi: 10.1016/j.saa.2013.04.129. Epub 2013 May 16. PubMed PMID: 23747387. 3: Ishida S, Mochimaru H, Nagai N, Noda K, Ozawa Y. [Effects of carteolol hydrochloride on experimental choroidal neovascularization]. Nippon Ganka Gakkai Zasshi. 2011 Apr;115(4):355-61. Japanese. PubMed PMID: 21598603. 4: Kaji Y, Kiuchi T, Oshika T. Carteolol hydrochloride suppresses the generation of reactive oxygen species and rescues cell death after ultraviolet irradiation of cultured lens epithelial cells. Open Ophthalmol J. 2010 Oct 12;4:60-5. doi: 10.2174/1874364101004010060. PubMed PMID: 21283534; PubMed Central PMCID: PMC3031156. 5: Kawase K, Yamamoto T, Muramatsu T, Ono J, Nakajima T, Matsuhisa A, Sugiura T, Migita M, Ishikawa Y. [Long-acting carteolol hydrochloride 2% ophthalmic solution phase IV study--investigation of the effectiveness, safety and plasma concentration]. Nippon Ganka Gakkai Zasshi. 2010 Nov;114(11):976-82. Japanese. PubMed PMID: 21141077. 6: Nakamoto K, Yasuda N. Effect of carteolol hydrochloride on 24-hour variation of intraocular pressure in normal-tension glaucoma. Jpn J Ophthalmol. 2010 Mar;54(2):140-3. doi: 10.1007/s10384-009-0780-6. Epub 2010 Apr 18. PubMed PMID: 20401563. 7: Shapiro MK, Gorn R. The possible treatment of migraine with carteolol hydrochloride. Headache. 1999 Feb;39(2):138-9. PubMed PMID: 18567128. 8: El-Kamel A, Al-Dosari H, Al-Jenoobi F. Environmentally responsive ophthalmic gel formulation of carteolol hydrochloride. Drug Deliv. 2006 Jan-Feb;13(1):55-9. PubMed PMID: 16401594. 9: Kuwahara K, Oizumi N, Fujisawa S, Tanito M, Ohira A. Carteolol hydrochloride protects human corneal epithelial cells from UVB-induced damage in vitro. Cornea. 2005 Mar;24(2):213-20. PubMed PMID: 15725891. 10: Kawai K, Kuwahara K, Oizumi N, Kitagaki H, Fujisawa S. Effects of carteolol hydrochloride on the in vitro production of LPS-induced proinflammatory cytokines by murine macrophage. J Ocul Pharmacol Ther. 2004 Jun;20(3):237-45. PubMed PMID: 15279728.
High Quality API Carvedilol Phosphate Hemihydrate Powder Best Price Carvedilol phosphate is a kind of selective blockade alpha 1 - receptor and nonselective beta blockers, no inherent to the sympathetic activity drugs, bioavailability of 10 ~ 47%, and is not affected by food, significantly lower than the action of the alpha 1 - receptor beta 1 - and 2 - receptor beta, the block 1 - and the strength of the beta 2 - receptor beta ratio of 1:10 ~ 1:100, block 1 - the role of receptor beta about 1/2 of labetalol and its weak prazosin alpha 1 block effect. It can dilate blood vessels, reduce peripheral vascular resistance, dilate coronary arteries and renal vessels, and reduce pulmonary wedge pressure. It has obvious protective effect on myocardial injury caused by myocardial hypoxia and myocardial infarction, which may be related to blocking -receptors, reducing the decrease of myocardial glycogen and the increase of pH, and reducing the infarct area. Function Carvedilol phosphate is used to treat mild to moderate hypertension and can be used alone or in combination with other antihypertensive drugs (especially thiazide diuretics). For symptomatic chronic congestive heart failure. Carvedilol has strong heart and neuroprotective effects: unlike normal β-receptor antagonists, long-term use of this product in hypertensive patients can not only dilate coronary and renal vessels, reduce peripheral vascular resistance, but also reduce systemic circulation. And pulmonary circulation resistance, effectively control high blood pressure. This product has a protective effect on renal function, does not change renal blood flow, but reduces microalbuminuria, reduces renal vascular resistance, and has a good regulatory effect on blood lipids.
Acer Therapeutics’ Edsivo (celiprolol) is not expected to win approval from the US Food and Drug Administration (FDA) for vascular Ehlers-Danlos syndrome (vEDS), as the registrational trial was too small and not well-controlled, according to experts.Celiprolol

Ehlers-Danlos syndrome treatment

EDS is a group of rare inherited conditions that affect connective tissue, of which vEDS is a rare type that is often considered to be the most serious. It affects the blood vessels and internal organs, which can cause them to split open and lead to life-threatening bleeding, according to the National Health Service.

An analyst report was optimistic about Edsivo’s FDA approval. It noted the previous data, as well as the fact that the drug is used as an off-label treatment in Europe and there is an unmet need in the US.Celiprolol is approved as a beta-blocker for hypertension. However, while one expert interviewed expressed hope for approval based on off-label use and unmet need, she declined to comment on the data’s validity.

Trial size too small

Other experts interviewed said that given the trial comprised of 53 patients, the Phase IV trial (NCT00190411) was too small even for a rare disease like vEDS.Furthermore, far fewer patients were recruited than the initial number needed to power the trial appropriately, said one of the experts.

Additionally, many more patients with the collagen 3A1 (COL3A1) gene mutation was in the control group with no beta blockers rather than the Edsivo group, said the experts.The COL3A1 mutation defines patients with vEDS, and thus non-vEDS patients may also have been included in the trial, one of the experts noted.

In terms of safety, while all the experts agreed that the trial results showed no red flags, two pointed to recently presented mouse data showing that Edsivo may increase death. While the data gave one of them pause, another expert cautioned on translating those results to humans.

Acer submitted a New Drug Application (NDA) to the FDA in October 2018 and has requested priority review for Edsivo, which could result in a late second quarter 2019 FDA review date, according to a company press release.Sales are predicted to reach $400 million, according to the analyst report. Acer’s market capitalisation is $239 million. Acer declined an invitation to comment for this article.

Efficacy data not robust enough

The study that the approval of Edsivo would be based on was not well-designed, with an overall small trial size, said vEDS expert Dr Harry Dietz, Co-director of the Medical Genetics Fellowship Training Programme and Professor of Paediatrics at The Johns Hopkins Hospital, Baltimore, Maryland, US.Only 53 patients were enrolled in the trial, indicating recruitment was likely to have been challenging, said Dietz, pointing out the trial was almost half the size that was initially targeted.

Lancet paper findings

The trial powering was based on enrolling at least 50 vEDS patients in each group, as 40 primary events were needed to achieve a power of 80% as cited in the Lancet paper where the study is published (Ong, K. et al. 2010 Oct 30; 376 (9751): 1476-84).

Additionally, the number of patients with vEDS is very low, which may have been the reason why so few patients were enrolled in the study, said Dr Paul Grossfeld, Pediatric Cardiologist with the Rady Children’s Hospital, San Diego, California and Francesca Cortini, PhD, Research Fellow at the University of Milan, Italy.The Lancet paper stated that there were 87 individuals eligible for the study but 12 refused to participate and four were unable to move.

Eighteen subjects who were previously treated with beta blockers were included in the follow-up cohort. The frequency of vEDS is estimated to be 1 in 50,000 to 1 in 200,000 (Am J Med Genet C Semin Med Genet. 2017 Mar; 175 (1): 40-47).While the major adverse cardiovascular events (MACE) primary measure is clinically significant, it can pose difficulties in recruiting patients, as an aortic dissection over five years is difficult to find, said Dr Grossfeld.

The MACE outcome measure in the clinical trials is a composite of clinical events that occur in patients. The Lancet paper stated that the reduction in the MACE primary outcome measure at a five-year follow-up was reached by five (20%) in the Edsivo group and by 14 (50%) controls (hazard ratio 0.36; 95% confidence interval [CI]; p=0.04), which is not a sufficient set of data to gain FDA approval, according to Dr Dietz and Dr Grossfeld.The results indicate there were more patients on the placebo arm who had aortic rupture than the Edsivo arm, the expert added.

Besides the low patient figures, the imbalance between the experimental and control arms in terms of patients with the COL3A1 mutation means the results are also insufficient for FDA approval, said Dr Dietz and Dr Grossfeld.Another study with the same number of patients with the mutation in each group or higher for both groups would be needed to identify the true Edsivo effects.

In the treatment group, 53% of the 25 patients in the Edsivo group had the mutation, while in the placebo group, 71% out of 28 patients had the mutation, the Lancet paper reported.A trial that compares only patients with the COL3A1 mutation to placebo patients can best identify any clinically significant benefit with Edsivo, said Dr Grossfeld.

Furthermore, when patients do not have the COL3A1 mutation but exhibit similar symptoms, then they may have another disorder such as Loeys-Dietz syndrome. Therefore, some of the trial’s patients may have not even had vEDS.

In its press releases, Acer has not indicated another trial would be run; rather it says the data in the Lancet paper, with an Acer-sponsored retrospective source verified analysis of the trial data and manufacturing, non-clinical and other components of the regulatory package, will go into the NDA.

While Ms Cortini did not comment on the results’ potential to trigger FDA approval, she said she hoped Edsivo would be approved, as it has been used in Europe as an off-label treatment. In fact, she noted, it is the standard of care for vEDS in France.
Used to strengthen the immune system, antibacterial role.
-Motherwort extract is valuable in the stimulation of delayed or suppressed menstruation, especially where there is anxiety or tension involved.Antiaging Powder
-Motherwort extract is a useful relaxing tonic for aiding in menopausal changes. Motherwort extract contains Leonurine which is a uterine stimulant.
-As well known, as a supplement designed for promoting natural breast enlargement and female breast enhancement.
-Motherwort extract can slow down the heart rate, against experimental myocardial ischemia and arrhythmia, anti-anginal and reduced myocardialinfarct size.
-A role in the treatment of acute renal failure, motherwort can improve renal function, Leonurine significant diuretic effect.

Application:
-Applied in food field, boiled eggs with motherwort is a good way to treat dysmenorrheal.
-Applied in health product field, motherwort honey is a good female health food, which helps to regulate menstruation nourishing.
-Applied in pharmaceutical field, motherwort tablets, granules, injection, capsule medicine for the treatment of gynecological diseases.
-Applied in cosmetic field, motherwort can be used as beauty products to make some one looks younger

Packing: Packaged in the net vacuum aluminum foil bag then packed in carton.
Storage: Keep tightly sealed. Stored in a cool dry place, protected from light, heat and oxygen. The preferred temperature is below 10℃ after open it.
Nootropic Powder J147 CAS 1146963-51-0 with Top Quality



J 147 is a novel neurotrophic drug for cognitive enhancement and Alzheimer's disease. J147 is an exceptionally potent, orally active and broadly neuroprotective compound has the ability to enhance memory in normal animals as well as to prevent memory deficits in Alzheimer's disease (AD) transgenic mice. The neurotrophic and memory-enhancing activities of J147 are associated with an increase in brain derived neurotrophic factor (BDNF) levels and the expression of BDNF responsive proteins, the enhancement of LTP, the preservation of synaptic protein, the reduction of amyloid plaques.
147 (CAD-031) is a Curcumin and Cyclohexyl-Bisphenol A (CBA) derivative that is a potent neurogenic and neuroprotective drug. It was developed for the use of treating neurodegenerative conditions associated with aging.

Unlike the current drugs approved for Alzheimer's Disease, J147 is neither an acetylcholinesterase inhibitor nor a phosphodiesterase inhibitor, yet it enhances cognition with a short-term treatment. J147 can cross the BBB into the brain (strong) and induce neuronal stem cell production.
Function:

Enhance mental intelligence; Boost memory and leaning capabilities;Improve brain power to solve problems and protect it from any chemical or physical injury;Enhance motivation level;Enhance the control of cortical/subcortical brain mechanism;Improve sensory perception.
Glutathione Skin Whitening is a tripeptide that contains an unusual peptide linkage between the amine group of cysteine and the carboxyl group of the glutamate side-chain. Glutathione Skin Whitening is an antioxidant, preventing damage to important cellular components caused by reactive oxygen species such as free radicals and peroxides.Alpha-lipoic Acid

Freeze-dried powder:
A sterile injection made by freezing liquid into solid state under aseptic environment and sublimating water to dry under vacuum is a physical state of a component rather than a component.

Vitamin c:
Natural antioxidant, used to prevent and treat skin sunburn, prevent melanin precipitation, whitening, freckle removal, anti-inflammatory effect.
1. Fast decomposition of melanin in human skin, whitening skin
2. Improve that facial spot and prevent melanin formation
3. Repair damaged cells and delicate skin
4. Inhibiting cell oxidation
5. Promoting Metabolism
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