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Wednesday, November 5, 2014

安成 AC-201(Diacerein) 多方進擊(痛風/水皰症epidermolysis bullosa) 巧取美國市場 !

The Pathogenetic Role of IL-1β in Severe Epidermolysis Bullosa Simplex

Journal of Investigative Dermatology (2013) 133, 1901–1903; Dominantly inherited epidermolysis bullosa simplex type Dowling-Meara (EBS-DM) is caused by mutations in either the keratin 5 (K5) or the keratin 14 (K14) gene, which encode the major components of the intermediate filament (IF) network in basal keratinocytes. In healthy keratinocytes, heterodimers of K5 and K14 polymerize to form a cytoplasmic network extending to the cellular periphery and imparting stability to the basal layer of the stratified epithelia. In EBS-DM, causative mutations lead to disintegration and collapse of the IF network, which manifests cytologically as electron-dense aggregates at the periphery of the keratinocyte cytoplasm (Morley et al., 2003). EBS-DM cells exhibit increased fragility to mechanical stress as well as to heat and osmotic shock, making Dowling-Meara the most severe subtype of EBS. As a consequence, EBS-DM patients suffer from blistering and wounding of the skin and mucous membranes after even minor trauma (Stephens et al., 1993; D'Alessandro et al., 2002; Coulombe et al., 2009; Jerabkova et al., 2010). Interestingly, upregulation of K14 at both the transcriptional and protein levels was shown recently in EBS-DM keratinocytes (Wally et al., 2010; Beriault et al., 2012). The JNK/MAPK stress pathway is also known to be upregulated in EBS-DM keratinocytes, and the cells show elevated JNK phosphorylation compared to clinically milder, K14-based EBS subtypes (D'Alessandro et al., 2002). Particularly with regard to a small molecule-based therapeutics, we have focused on the pathomechanism underlying K14 overexpression and aggregation. We have investigated the potential involvement of the pro-inflammatory cytokine IL-1β in EBS-DM pathology. IL-1β is secreted by keratinocytes (and other cell types) and binds to specific receptors of basal keratinocytes, activating those cells in response to wounding. Activated keratinocytes exhibit higher migratory potential and hyperproliferative activity, and secrete extracellular-matrix components and signaling polypeptides to the tissue microenvironment (Freedberg et al., 2001). Defects in these processes could also contribute to the EBS-DM phenotype. To summarize, we showed here that, in EBS-DM keratinocytes, IL-1β signaling is constitutively activated, resulting in activation of the JNK stress pathway and overexpression of K14 and IL-1β itself in a positive feedback loop. Through this mechanism, expression of the dominantly interfering mutated K14 allele would also increase, potentially aggravating the EBS-DM phenotype. Therefore, therapeutic approaches to interrupt this positive feedback loop by inhibiting IL-1β using a neutralizing antibody or diacerein would seem worthwhile. Indeed, treatment of patient keratinocytes with these agents not only reduced the expression levels of K14 and IL-1β and the phosphorylation levels of JNK, but also stabilized the IF network upon heat shock. Our data are further corroborated by our recent demonstration that overall K14 expression levels in EBS-DM keratinocytes are reduced upon mRNA correction via spliceosome-mediated RNA trans-splicing (SMaRT), which shifts the expression ratio of wild-type versus mutated K14 alleles toward wild-type (Wally et al., 2010). We therefore propose that inhibition of IL-1β could be beneficial to EBS-DM patients by ameliorating the EBS-DM phenotype.

安成藥 獲美孤兒藥認定【經濟日報╱記者黃文奇/台北報導】2014.10.22 02:43 am安成藥(4180)昨(21)日宣布,子公司安成生物科技旗下用以治療先天性水皰症(epidermolysis bullosaEB)的產品AC-201,獲美國食品藥物管理局(FDA)孤兒藥資格認定。安成生技總經理陳志光表示,AC-201用於治療先天性水皰症,該疾病是一種非常罕見的基因突變疾患,換言之,即業界所謂「無適當醫藥可滿足現有需求」的疾病(unmet medical needs)。安成藥昨日股價收233.5元,上漲1.5元。據悉,該種疾病在美國,每5萬名新生嬰兒即有一例先天性水皰症病兒,目前估計在美國已有約3萬名病患,而在台灣也約有數百名病患有這種俗稱「泡泡龍」的惡疾,此疾棘手之處是輕微的摩擦就可能造成患者皮膚上的水泡或裂傷。陳志光表示,希望AC-201的孤兒藥的資格認定能加速此候選藥物的開發。陳志光指出,經皮吸收的AC-201劑型可能用來預防或減少水泡的發生,這樣就可以大大的減輕先天性水皰症患者及其家人的痛苦,因此安成生技也將開始進行AC-201經皮吸收劑型的臨床實驗的程序。【2014/10/22 經濟日報】

 

Topical diacerein for epidermolysis bullosa: a randomized controlled pilot study   Orphanet Journal of Rare Diseases 2013, 8:69  listering in epidermolysis bullosa simplex type Dowling-Meara (EBS-DM) is associated with an inflammatory phenotype, which can be disrupted by diacerein in vitro. In this pilot study we hypothesized, that a topical formulation of diacerein 1% reduces blistering. Five patients initially applied diacerein underneath both armpits. Then, each participant received 1% diacerein-cream for one armpit, and placebo for the other (randomized withdrawal). The number of blisters was reduced significantly (left: -78%; right: -66% of baseline) within two weeks and remained significantly below the initial level even during withdrawal in four patients. These findings point to a relevant effect of diacerein and provide important information for a confirmative study.

EBS-DM is the consequence of dominantly inherited mutations in either the keratin 5 (K5) or keratin 14 (K14) gene, which encode proteins constituting the intermediate filament (IF) network of basal keratinocytes. Mutations lead to an increased mechanical susceptibility of keratinocytes, manifesting in a collapse of the IF network [1]. Clinically, patients suffer from blistering of the skin upon minor trauma, resulting in an impaired quality of life due to pain and pruritus [2]. In vitro studies on EBS-DM keratinocytes showed a significant upregulation of interleukin-1beta (IL-1ß), resulting in the activation of the c-jun N-terminal-kinase (JNK) stress pathway and subsequently in the overexpression of K14 and IL-1ß in a positive feedback loop. When impairing IL-1ß signaling, using anti-IL-1ß antibody or the small molecule diacerein, levels of IL-1ß, JNK and K14 decreased and the IF network was stabilized [3]. Based on this information, we launched a double-blinded, randomized, placebo-controlled pilot study using a 1% diacerein in the commonly used care cream ultraphil® as intervening agent, and ultraphil® alone as placebo. Diacerein, a prodrug of the IL-1 converting enzyme inhibitor rhein, is approved for the systemic treatment of osteoarthritis (Verboril®) [4,5]. It is metabolized in the liver and cleared by the kidneys. Up to now there are no data available on topical application. To test our hypothesis that diacerein is able to reduce blister formation, we recruited five patients (aged 6 to 48) with the diagnosis of EBS-DM and a heterozygous amino acid exchange in K14 protein position 125. An a-priori sample size computation was done in consideration of a 0.90 power, a 5% significance level and a minimum difference between blister numbers of 30%. A 25% standard deviation for the intervention group and 15% for the placebo group was expected. Computation was done for a one-sided, paired student t-test. Including a 10% drop-out rate, the calculation resulted in ten armpits of five patients to be included (Figure 1A). Randomization was done using random numbers, with the general requirement that no patient receives placebo or diacerein on both sides. The two-phased study started with a six-weeks open phase (P1), where all patients received 1% diacerein cream to apply underneath both armpits every evening. Usual care was continued unchanged. Blister numbers were documented every second day by the patients and every second week by a study nurse, who visited the patients at their homes to avoid any influences from travelling or changes of habits. Furthermore, patients were requested to take photos of the blisters plus a tape measure to allow for software aided quantification of blister areas (Figure 1B). To optimize the strength of our small pilot trial we added a second, randomized, placebo-controlled six-weeks phase (P2), exploiting the fact that placebo and verum could be used in parallel in the same patient, which virtually doubled our sample size. Time to loss of efficacy (defined as halving the effect in P1) was chosen as primary endpoint, because this allows minimizing the time on placebo, as patients can be de-blinded and switched to verum as soon as loss of efficacy occurs. For data analysis, we sub-divided the study period into eight time intervals (t), each including six counts (Figure 1C). Patient DIDM005 (1965) did not develop blisters during the study, contradictory to an aforegoing patient inquiry on times of most strain. DIDM005 was therefore excluded from the statistical evaluation. However, it cannot be excluded that the absence of blisters is due to the treatment. As blister numbers are likely to be correlated (two measurements within the same subject), generalized estimation equations (GEE) were used. The group (verum/placebo) was the main effect and time*group was used as interaction effect. The robust method (Huber/White/sandwich estimator) was used for estimating the covariance matrix. Pairwise comparisons are based on the sequential Bonferroni method. The significance level was set to 5%. Results showed a statistically significant reduction of blisters within the first two weeks of P1 (t1: 100%, t2: mean left: 22%/CI6-38; mean right: 34%/CI20-48), which remained stable until the end of the study period (Figure 2A). In P2, we could not observe any loss of efficacy and missed our primary endpoint. Although the relative number of blisters was slightly higher on the placebo sides, there was only a statistically significant difference at t7 (Figure 2B). We believe that carrying-over of the positive effect from P1 into P2 is the reason for that observation. Thus, unless missing the primary statistical objective, the results point to a beneficiary effect of diacerein.

痛風意味高機率陽痿與心血管疾病!!

Gout diagnosis an important opportunity to detect possible silent coronary artery disease  Last updated: 15 June 2014  A new study presented at the European League Against Rheumatism Annual Congress (EULAR 2014) showed that erectile dysfunction (ED) is present in most men with gout and is frequently severe.1 In a survey of 201 men, 83 had gout, of whom a significantly greater proportion had ED (76%) compared with those patients without gout (52%) (p= 0.0007). Also, a significantly greater proportion of gout patients (43%) had severe ED compared with patients without gout (30%) (p=0.007).1According to lead author Dr. Naomi Schlesinger, Chief, Division of Rheumatology and Professor of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, US, "these results strongly support the proposal to screen all men with gout for the presence of ED. Increasing awareness of the presence of ED in gout patients should in turn lead to earlier medical attention and treatment for this distressing condition," she added.Gout is a condition characterised by recurrent attacks of acute inflammatory arthritis. Around 1-4% of the Western population will develop gout at some point in their lifetime.2 The arthritis is caused by deposits of needle-like monosodium urate crystals in the joints and is associated with an abnormally high level of urate in the bloodstream. The crystals cause inflammation, swelling, and pain in the affected joint.2 "Because gout is commonly associated with cardiovascular disease (CVD) risk factors and coronary artery disease (CAD) and patients who present with ED also have an increased rate of CVD risk factors and concomitant silent CAD, all these patients should also be evaluated for possible silent CAD," Dr. Schlesinger concluded.ED is a common problem in the general population, with the prevalence of moderate to severe ED estimated to between 5- 20%.2 The likelihood of ED increases progressively with age; however, it is not an inevitable consequence of aging.3 The importance of vascular disease as an underlying cause of ED is well established.2In this cross sectional study, men aged 18-89 presenting to a Rheumatology clinic between August 2010 and May 2013 were asked to participate. The presence of ED was determined by filling out a Sexual Health Inventory in Men (SHIM). The SHIM classifies ED into one of five categories: absent (26), mild (22), mild to moderate (17), moderate (11) and severe (1). The patient's history, physical examination and recent laboratory studies were reviewed as well. Descriptive statistics and subgroup analyses were used to summarise the data. Chi-square tests for independence were used to compare categorical variables.The mean SHIM score of all patients was 16.88 (SD±-0.83). Gout patients had an average SHIM score of 14.38 (SD±1.01) vs. 18.53 (SD± 0.964) in patients without gout (p < 0.0001). A significantly greater proportion of gout patients whose age was ? 65 had ED vs. patients without gout (p=0.0001) and it was significantly more likely to be severe ED vs. patients without gout (p=0.0002). A significantly greater proportion of patients with tophaceous gout* had ED vs. those without tophi (p=0.0001). In a multivariate analysis, the association between gout and ED remained statistically significant even after adjusting for age (p=0.0009), hypertension, LDL-cholesterol, glomerular filtration rate (a measure of renal function), obesity, depression (p=0.0154) and diabetes (p=0.0085).

AstraZeneca 痛風藥lesinurad 將成複合治療(cocktail) 主基調?!

AstraZeneca may have a gout blockbuster on its hands with lesinurad   February 14, 2014 | By Damian Garde With the rates of gout on the rise throughout the world, AstraZeneca ($AZN) and its Phase III therapy lesinurad could be lined up for a lead role in a growing market, welcome news for the sluggish pharma giant and its thin late-stage pipeline. As Bloomberg points out, the disease is on the rise in the West, afflicting 8.3 million Americans by 2011 and increasing 64% in the U.K. from 1997 to 2012, and roughly 17.7 million patients are expected to come down with gout by 2021, according to a study. Meanwhile, current treatments are limited to the 50-year-old generic allopurinol and Takeda and Ipsen's ($IPN) febuxostat, a drug approved in 2009 that doesn't work in every patient, the news service notes. That sets the stage for AstraZeneca and its promising lesinurad. The drug is a selective uric acid re-absorption inhibitor that blocks the URAT1 transporter, treating the painful condition by normalizing acid excretion and reducing serum levels. In top-line results from a Phase III study on gout patients who get no benefit from allopurinol and febuxostat, lesinurad alone significantly reduced serum levels of uric acid, AstraZeneca said. But what has analysts optimistic that lesinurad can cross the $1 billion threshold is the promise of combo treatments. AstraZeneca is in the midst of three more Phase III trials to suss out how the drug works in tandem with allopurinol or febuxostat, expecting to report data by mid-year. If those go well, a cocktail led by lesinurad could become a go-to treatment for physicians around the world, giving AstraZeneca a standard-bearing treatment for a growing global scourge. Standing in its way, however, are some alarming safety issues that could spell trouble once lesinurad has its day at the FDA. In the Phase III monotherapy trial, the drug increased patients' risks of kidney trouble and led to a few serious adverse events, the company said, withholding specifics but saying that other side effects included diarrhea, nausea and constipation. Analysts will certainly be keeping an eye on any kidney risks with each new spate of Phase III data.  

 

慢性痛風 不僅是 痛風/ 忽略難回頭

Gout: Obesity's Stealth Disease Published: Jan 21, 2014 | Updated: Jan 22, 2014 By Nancy Walsh , Staff Writer, MedPage Today Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner The incidence of gout has been increasing considerably over the last several decades. The cornerstone of therapy is urate-lowering therapy with a xanthine oxidase inhibitor, usually allopurinol targeting a serum urate level of less than 6 mg/dL. Once known as "the disease of kings," gout today clearly is a disease of commoners as well, and although it's on the rise, treatment remains vastly underused. A recent estimate of the prevalence of gout in the U.S. set the number at about 8.3 million, or 3.9% of the population. "There are data suggesting that the incidence of gout in this country has doubled in the last 20 years and probably tripled in the past 40 years, making it by far the most common inflammatory arthritis," said N. Lawrence Edwards, MD, of the University of Florida in Gainesville. Reasons for this increase include the obesity epidemic, widespread use of medications such as diuretics that elevate urate levels, and greater longevity. "Historically, gout has been associated with overindulgence, in people who had access to foods of plenty, but now, in fact, gout is a condition of people with chronic illness such as kidney disease and heart disease, and regrettably it's often relegated to a lesser status given all the other challenges of management," explained Kenneth S. Saag, MD, of the University of Alabama at Birmingham. In a recent U.K. survey, only one in four patients with a new diagnosis of gout initiated urate-lowering therapy within a year. And among patients taking urate-lowering treatments, only 40% were adherent. This can have serious consequences, since increasing evidence is demonstrating that gout contributes significantly to the burden of cardiovascular morbidity and mortality.

A Disease of Misperceptions The most important hindrance to effective treatment of gout is the misperception by both clinicians and patients that it's an acute, intermittent -- and painful but relatively inconsequential -- disease rather than a chronic, destructive form of arthritis. "We now know that crystals are present in the joint long before the first symptomatic episode of gout, and that there's low-grade inflammation destroying the joint," Edwards told MedPage Today. "Because of a lack of appreciation of that destructive nature, many primary care physicians and even some rheumatologists are willing to just treat the acute attacks with the old standards of nonsteroidal anti-inflammatory drugs or colchicine and let it go at that," he added. However, gout today is considered largely curable and very effective treatments are available. "It's one of the few conditions in medicine where we know the cause and we can offer therapies that, if initiated early and used appropriately, can essentially fully reverse the process," Saag said in an interview. That process results from persistent levels of uric acid above the level of saturation and leads to crystal formation in the joints and soft tissues. When the monosodium urate crystals reach the joint space or bursa, the NALP3 inflammasome is activated and cytokines such as interleukin-1 and tumor necrosis factor are released, resulting in the acute episode.

Poor Use of Allopurinol Various groups including the American College of Rheumatology (ACR), the British Society for Rheumatology, and the European League Against Rheumatism have offered guidance for the treatment of gout. The cornerstone, according to all the recommendations, is urate-lowering therapy with a xanthine oxidase inhibitor, usually allopurinol. The ACR guidelines state that urate-lowering therapy should target a level below 6 mg/dL, and for some patients, below 5 mg/dL, starting with a low 100-mg-per-day dosage. Many physicians initiate therapy by just giving a set dose of allopurinol, typically 100 mg or 300 mg/day, depending on kidney function. "For years we used allopurinol poorly, and we still use it poorly," said Edwards, who heads the Gout and Uric Acid Education Society. Too often, clinicians assume that once they have given the patient a prescription for allopurinol, there's nothing else they can do. In fact, allopurinol can be escalated as high as 800 mg per day. The right dose for any given patient is the dose that gets their uric acid below 6 mg/dL, according to Edwards. And further, many clinicians never even go back to measure the uric acid after initiating treatment. "That's like starting them on metformin for diabetes and not checking to see if it's doing any good," he said. An additional reason for the underdosing of allopurinol has been concern about the potentially lethal systemic hypersensitivity reaction that occurs in about one in 500 to 1,000 new patient starts, usually in patients with kidney disease. The chance of this can be minimized by starting with the low dose, Edwards noted. The ACR guidelines also recommend that individuals at high risk for the hypersensitivity reaction, such as those with Han Chinese and Thai ancestry, undergo screening for the predisposing HLA-B*5801 allele. Patients who are unable to tolerate allopurinol today have an alternative in febuxostat. The ACR guidelines state that either allopurinol or febuxostat (Uloric) can be used first line, but febuxostat is more expensive, and in practice allopurinol is typically the favored option.

Urate and Consequences If unchecked, elevated serum urate can lead to an exceptionally disabling chronic arthritis that's associated with pain and the loss of ability to work or participate in normal activities of daily living, according to Saag. But it's now becoming clear that elevated urate -- even in the pre-gout stage -- is associated with other conditions, including hypertension, coronary heart disease, myocardial infarction (MI), and kidney disease, so there's increasing interest in trying to prevent or moderate elevated serum urate, Saag explained. And evidence is emerging that the association is independent of shared risk factors. For instance, in one report of men enrolled in the Health Professionals Follow-up Study, the relative risks for all-cause mortality, cardiovascular death, and fatal coronary heart disease among men with gout were 1.28 (95% CI 1.15-1.41), 1.38 (95% CI 1.15-1.66), and 1.55 (95% CI 1.24-1.93), respectively. "These associations were independent of age, body mass index, smoking, family history of MI, use of diuretics and aspirin, dietary risk factors, and risk conditions such as diabetes mellitus, hypercholesterolemia, and hypertension," the authors wrote in Circulation. In another prospective study conducted in Singapore, patients with gout had a 23% increased risk of all-cause mortality (HR 1.23, 95% CI 1.10-1.38), and 54% increase in risk for death from coronary heart disease (HR 1.54, 95% CI 1.23-1.93), and a seven times higher risk for death from renal disease (HR 7.21, 95% CI 4.48-11.60). "These associations were independent of major confounders in lifestyle and comorbidity factors, and were present in both men and women," the researchers stated. Serum urate also was linked with hypertension in young adults in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort, which followed almost 5,000 participants for 20 years. That study found a 25% greater likelihood of developing hypertension in men with elevated serum urate (HR 1.25, 95% CI 1.15-1.36) and a 12% increase with each mg/dL increase in serum urate (HR 1.12, 95% CI 1.02-1.20). Moreover, the greater risk of developing hypertension was seen even at levels of serum urate below the threshold of 6.8 mg/dL, which is a generally accepted definition of hyperuricemia. For men, the increased risk began at levels of 5.80 mg/dL, and for women, at 3.60 mg/dL. "Our findings are in concordance with the growing body of data that supports a potentially causal role for elevated serum urate in the development of hypertension," Saag and colleagues wrote in Annals of the Rheumatic Diseases. Most recently, a group of French investigators found a 20% decreased risk of nonfatal first myocardial infarction in patients with gout treated with allopurinol. In their report, published online in Annals of the Rheumatic Diseases, the French researchers noted that uncertainty remains as to the precise mechanisms that link elevated urate with cardiovascular disease, "but may include oxidative stress generated by xanthine oxidase, the enzyme that catalyzes the formation of urate." "Indeed, allopurinol, a free radical scavenger, was found to improve both endothelial dysfunction and levels of some markers of oxidative stress," they observed. They called for randomized studies to directly assess the effects of xanthine oxidase inhibition on cardiovascular outcomes among individuals with gout.

 

電子業英濟如何整合跨入生技: 整合式行銷 & 健康管理 & mHealth !!

保健食品廠 喜訊一波波 2014-10-06 經濟日報 記者/黃文奇 台灣保健食品廠大江生醫、F-麗豐、電子元件廠英濟轉投資的聯邦應用基因,近期陸續傳出好消息,其中,大江將獲大同藥品母公司DYDO(大德食品)參股,參股比重約9%10%,大江將於今(6)日召開股東臨時會討論私募入股案。無獨有偶,麗豐與大陸電子商務巨擘天貓合作的O2O模式,其減重瘦身產品將在近期同步在大陸開賣;英濟轉投資的聯邦應用基因,其健康管理保健套組近期也將在大陸推出。大江對私募案表示,雙方仍在討論中,但公司與大同藥品早已是合作夥伴,未來若該母公司入股,則是進階合作,因此樂觀其成。至於麗豐,該公司旗下美容保養飲品「百奧維他」,近期將在大陸電子商務網站天貓上架。麗豐表示,這是一套自家開發的35天果汁搭配蛋白粉的療程,飲品是與瑞士夥伴攜手引進的「Biotta」果汁,蛋白粉則由全豐盛集團旗下子公司佰研開發生產,一套療程約人民幣1.2萬元。麗豐表示,近期在天貓上推出的健康美容產品組,需要搭配「諮詢師」,進行35天健康飲食、三天斷食的排毒療程,近期已啟動招募諮詢師,10月即將開始銷售。值得注意的是,英濟轉投資的聯邦應用基因旗下的「健康管理套組」也將在大陸上市,主要針對大陸廣大的女性族群,協助完成個人化健康管理減重目的,包括基因檢測、體型評估、產品推薦、運動建議等,一條龍的客製化服務。英濟為33年的老牌科技周邊元件開發公司,目前資本額約13億元,兩岸皆有廠,近期積極跨入生醫領域,並已有初步規模;聯邦應用基因由英濟持股五成以上,股本約1億元,為個人化、預防醫學專業公司。營業模式方面,英濟董事長徐文麟說,公司將打造一個「差異化、客製化、個人化」醫療系統,聚焦預防醫學,用基因檢測方式,搭配健康食品銷售模式,在大陸發展直銷體系,10月間將有具體成果。線上諮詢師 服務客製化智慧健康保健食品的商業模式,不僅強調客製化,也重視互動,英濟轉投資的聯邦應用基因、F-麗豐,近期將在大陸推出保健品銷售組合,不約而同都建立線上真人「諮詢師」團隊,不僅賣產品,也要賣服務。英濟董事長徐文麟表示,公司此次推出的客製化體重控制產品,不僅可能找兩岸知名藝人代言,更重要的是,每個購買的客戶,都會有專屬諮詢師,協助消費者完成體質檢測、產品配方組合、課程安排與規劃,透過雲端的監測與互動,讓消費者能知道如何運動,更快達到減重瘦身的目的。麗豐則透過線上諮詢師,在消費者購買產品後的35天內,協助消費者如何吃的正確;麗豐表示,諮詢師未來都會由台北醫學大學的專業團隊訓練,結訓後還會有證書,近期就可以上線服務。據悉,麗豐的體重控制產品「百奧維他」,消費者可在網路下單、鍵入基本資料後,麗豐方面會就近派出專屬諮詢師,這個諮詢師會主動聯繫購買人,未來這個諮詢師也是銷售窗口,只要消費者多買一個產品,諮詢師將有新一筆收入。業界認為,現在保健食品不再是「以量取勝」的銷售策略,而是透過專人、專屬、客製化的服務模式,來滿足特定客群的需求,這樣的生意模式將成為兩岸華人健康食品主流。

科技元件大廠英濟 跨足行動醫療【經濟日報╱記者黃文奇/台北報導】2014.07.23 02:46 am科技元件大廠英濟(3294)董事長徐文麟昨(22)日宣布,公司將進行轉型、跨足生技醫療產業,第4季將在兩岸推出具備「健字號」的體重控制健康食品,本業也將打造電子穿戴裝置的「行動醫療」領域。近期,徐文麟投資生技公司「聯邦應用基因」,由英濟持有五成以上,股本約1億元,為個人化、預防醫學專業公司。英濟昨日股價收13.9元,上漲0.05元。徐文麟說,未來將打造從「健康雲、穿戴裝置、基因檢測到健康控制方案,一直延伸到健康產品」等,一條龍客製化服務,由頭至尾都由英濟自己建置、產品自己生產,建構完整的健康管理方案,大陸市場將攜手對岸夥伴於下季推出。對於跨入醫療領域,徐文麟表示,公司在30年早跨入醫療有關領域,並與國際大廠惠普(HP)合作,此次「轉型」其實是本業的延伸,近期,公司已經和國內生技醫療公司合作,將生產「呼吸道」治療周邊產品。此外,徐文麟也透露,公司未來不排除跨入「高階醫材」,如第三類的植入性醫療器材,目前已經透過由國科會(今科技部)、美國史丹福大學共同成立的「史丹福醫療器材產品設計人才培訓計畫(STB)」,並與該計畫中歸國的醫療人才合作,開發嶄新的醫材產品。 2014/07/23 經濟日報】

聯邦應用基因股份有限公司 (Union Applied Gene Inc.)為上櫃電子公司的轉投資事業,以現有的電子化平台跨入生物科技產業,我們深信,個人化健康管理是未來預防醫學的主要趨勢,而跨領域的整合更成功的不二法門。UAGI 結合科學研究及健康產品專業,致力於整合醫療及健康相關研究,利用先進的生物技術建立個人化健康管理系統並發展相關產品。UAGI 將以產業落實導向的特有營運模式,確實將最新生物科技應用到個人健康生活中。 

本公司目前旗下相關產業包含: ~ 診所諮詢顧問管理 ~ 自然醫學健康事業 ~ 健康保健食品開發 ~ 電子商務平台開發  ~ 行動裝置開發。UAGI 結合各方的產業力量,以專業分工的背景強化公司能量,多角化發展,使公司運作效率化。我們歡迎具有靈活創意的菁英分子加入我們的行列。 主要商品/服務項目 1. 個人化健康風險管理服務 2. 個人化醫療器材開發 3. 個人化醫療服務整合 4. 診所連鎖顧問管理

大江 機能飲料 將採台灣代工 日本品牌策略 (轉代工)

大江與日本大同藥品結盟 林詠翔:站在巨人肩上共同成長! 鉅亨網記者 胡薏文 台北 | 鉅亨網  201448 下午8:45 大江生醫(8436-TW)與日本第一大機能飲料代工廠商大同藥品,今天下午簽署合作備忘錄,合作範圍包括技術移轉以及委託代工部分。大江也是日本大同藥品亞太地區第1家簽署戰略合作伙伴,雙方將聯手進軍台灣、大陸市場。大江生醫總經理林詠翔表示,這項戰略結盟,是讓大江「站在巨人肩上共同成長」!同時雙方也不排除未來更進一步邁向「資本合作」。 大江生醫今天與DyDo Drinco的全資子公司大同藥品工業株式會社,簽署戰略合作備忘錄。由於大同藥品為日本第一大機能飲料代工廠,客戶涵蓋資生堂、DHC、武田等100多家品牌廠商,在日本機能飲料市占率達5成,每年產量約3.2億瓶,此次為大同藥品使首度與海外廠商結盟,且雙方未來也將以大同藥品現有的日本企業客戶,進行健康食品、飲料的銷售,共同開發台灣、大陸等新市場,也使得此一中日保健飲料合作案,備受業界矚目。 大江生醫表示,與大同藥品合作的首款產品,目前正在緊鑼密鼓進行中,今年度將可在台灣上市,而大陸市場部分,由於大陸廠第4季才可完工,也不排除先由台灣生產,再運往大陸銷售,大陸市場部分,明年將有較大規模的銷售量。大江預估雙方合作後,兩岸市場年出貨量將有機會上看500-1000萬瓶,占整體營收比重約1成。 林詠翔指出,大江與日本大同藥品的結盟,為長期深度戰略合作,除了技術移轉以及委託代工外,大同藥品採購大江生產的原料,也在討論範圍中,而雙方的合作基於產品線互補,且大江的研發能力,也獲得大同藥品看重,雙方合作是讓大江「站在巨人肩上共同成長」,進而連結全球市場。   

大江攜日大同藥品 攻陸健康食品飲料 20140409日瞄準兩岸商機,大江生醫昨與日商大同藥品簽署備忘錄,將共同進軍中國健康食品和飲料領域。圖為董事長楊武男。蕭榕攝 【黃馨儀╱台北報導】瞄準兩岸市場商機,大江生醫(8436)昨與日本機能性飲料代工龍頭大同藥品工業株式會社簽署備忘錄,未來將合作進軍中國的健康食品和飲料市場。 大江生醫董事長楊武男表示,這不僅是大同藥品首度與外結盟,也創下台、日保健飲品合作新頁;法人表示,除今年有新品上市,明年若成功進軍中國,中國出貨量可望上看500~1000萬瓶。

日藥廠 大同藥品(DAIDO PHARMACEUTICAL) 參與 大江私募5千張(9%) !!!

親上加親!大江(8436)私募引進大同藥品,成單一最大法人股東2014/08/28 11:57

 【財訊快報/何美如報導】大江生醫(8436)4月攜手日本大同藥品工業,雙方建立全方位合作後,近日公告擬辦理私募5千張,每股暫訂71.5元,應募人即為大同藥品,未來將成大江的單一最大法人,法人預期,未來雙方將更無保留的合作,共同進軍中國及東南亞市場,對大江的業績貢獻可望在明年開始顯現。大江生醫日前公告,擬辦理5千張普通股私募案,預計參考價格暫訂為新台幣71.5元,應募人為大同藥品(DAIDO PHARMACEUTICAL CORPORATION)及其母公司大德飲料(DyDo DRINCO, INC.),以大江目前5.1億元計算,私募後股本將增為5.6億元,大同藥品將持股近9%,成為單一最大法人股東。此私募案預計在106日召開的股東臨時會通過。今年4月大江生醫已與大同藥品簽訂戰略合作備忘錄,雙方將就健康飲品及飲料事業,從原料研發設計、生產管理、市場開拓及委託生產等建立全方位的合作,以台灣市場為基地,並攜手進軍中國及其他海外市場。由於雙方在新市場、新品項的進行合作,配合大江上海廠的投產,效益最快明年才能顯現,但台灣廠今年將先承接既有品項訂單在台生產銷售。據了解,大同選擇參與大江私募,是強化上下游的佈局,並強化雙方在中國及東南亞市場拓展的合作。法人表示,大江若成功引進大同藥品成為股東,雙方將從技術、業務合作,進一步發展至資金合作,在親上加親下,未來合作案將更無保留的進行,成效將更顯著。

健保收入5557億元(2013) 仍窮?!

健保支出連年成長 就醫品質卻愈來愈差‧遠見 2014/10/03 自從19953月實施全民健保後,健保收入與支出從來沒有減少過,收入從第一年760億元增加到20135557億元,但健保署仍然喊窮,希望對企業與人民增收健保費,而醫護人員為何又沒蒙受好處,每個大喊「血汗醫院」,紛紛想轉換跑道。顯然制度設計與分配出了嚴重問題。 【文/彭漣漪】

現象1〉健保年收入增至5557億元,卻仍困難重重 自從19953月實施全民健保後,健保收入與支出從來沒有減少過,收入從第一年760億元增加到20135557億元,但健保署仍然喊窮,希望對企業與人民增收健保費,而醫護人員為何又沒蒙受好處,每個大喊「血汗醫院」,紛紛想轉換跑道。顯然制度設計與分配出了嚴重問題。19953月跟健保同一天開幕的桃園壢新醫院,創辦人張煥禎笑說:「我跟健保同年同月同日生,希望不要同年同月同日死!」一句話反映了對醫療環境的無奈。

現象2〉民眾每年就診15次,洗腎給付高達11.6 便宜又方便的健保,一次門診費用100300多元不等,把醫院當購物中心逛,昨天在台南成大醫院,今天到台中榮總,後天再到台大醫院……,幾百元就可以找遍台灣名醫。造成台灣人看病世界第一,平均每人每年門診15次。美國人不到4次、英國則是5次。健保花費攀升,就是因為給付項目愈來愈多,每年不斷新增,幾達包山包海、大小通吃,當然每一項給付就減少了。振興醫院心臟醫學中心主任魏崢指出,在還沒健保前,公保一條腿靜脈曲張手術費16000元,兩條腿乘以2。變成健保後,目前第一條腿開刀約剩4000元, 第二條腿手術就變12但魏崢指出,健保也有太過大方的地方。例如心臟裝個體內自動電擊器一裝50萬元,已經是買一台車的錢了。沒有給付前很少醫生幫病人裝,但一給付,馬上10倍、100倍在裝。再比較2013年與2004年,健保門診給付最多的前五大疾病,    在國外,洗腎病人的換腎比率是一半。如果台灣洗腎要自行給付一定費用,換腎比例一定會提高。件數最多的感冒(上呼吸道感染),從7230萬件減少為5300萬件,占比名次掉到第三。然而,等於每人每年要看兩次感冒,件數是所有疾病的第一名,花掉醫生不少的時間。歐美人很少感冒去看病,因為看病很貴,多半到藥局買藥、多休息喝水就好。

現象3〉醫院靠門診拚業績,住院病人誰來顧?1990年代健保設計時,原先是希望住院收入超過門診收入,但由於健保強調論件計酬精神,導致門診成為各大醫院的主要收入來源。一般而言,門診雖然賺小錢,但保證賺錢,而且之後的檢查都有一定給付。但病人若住院,一不小心可能就讓醫院賠錢,因此門診給付占醫療支出比率逐年增加,從66%(2002年)成長到69.6%(2013年)。連幾大教學醫院也必須加門診衝業績,不少紛紛加開黃昏門診、夜間門診、假日門診等。衝量下,讓有經驗的主治醫師疲於奔命看門診,病房內更嚴重的病人,就讓較資淺的住院醫師照顧,對於長遠的醫療環境是有害的。

現象4〉醫美勝過傳統醫療,整形醫師增加190前不久,醫生出身的立法委員蘇清泉跟記者開會時,語帶誇張地說,他就讀醫學系的兒子,同學們選科別,被歸到婦產科的同學們,一知道結果,馬上跪下來痛哭。近幾年台灣醫界出現「五大皆空」科,至今沒有好轉,因為沒有新手接班,目前40歲以上的資深醫師愈來愈累,年輕一輩紛紛轉去「沒有生命危險、少醫療糾紛、工時固定」的五官科及皮膚科,簡稱「五加皮」。2013年比上1998年,婦產科醫師數量只成長3%、外科多15%,然而,牙醫增加55%、皮膚科增加87%、整形外科則增加190%。台灣醫師數量到底夠不夠?與其他國家比較,每百床病床的臨床醫師數量,台灣只有27人,遠低於美國的79人、英國的92人、瑞典的38人。表示台灣醫師要照顧的病人數量遠高於其他國家。

現象5〉醫療變廉價,提供一元服務僅賺0.83 台灣健保總額是一定的。餅就這麼大,但醫療診治行為愈來愈多,因此設計出一套機制,讓每個醫療院所得到的給付打折。以西醫為例,20032013年間,平均點值最低掉到0.8635,近幾年也是逐年下降,今年第一季台北來到0.83。等於提供一元服務只能拿到0.83元。台北市就醫相對便利,造成醫療診治行為更多,壓低浮動點值。健保署也是有苦衷,總額就這麼多,但每年有新增加給付項目,各醫療院所的醫療服務業務又成長,只好想辦法刪減藥費、找出各家提供的哪些醫療服務有「瑕疵」,可以整筆刪除。結果,醫生做愈多卻給付減少,只好拚命做更多,總數可以拿更多。但當總數成長時點值就下降,大家只好又做更多,健保署再刪更多,成為惡性循環。

現象6〉醫療糾紛遞增,醫病關係雙輸 近幾年來讓醫界煩心的事除了辛苦外,還有醫療糾紛頻起。被病家天價索賠,已讓不少醫師退縮,病患親友在急診室痛打醫護人員的新聞頻傳,也讓醫師灰心。例如敏盛醫院副院長兼骨科部主任吳興盛就分享,他部門一位40多歲的骨科醫師因為一次醫療糾紛,「傷心」離開醫院,到坊間骨科小診所看診、打針就好,再也不碰開刀手術了。近幾年來醫療糾紛遞增,健保開辦當年只有194件,2012年已達524件。雖然最後一審被判有罪、有罪定讞的人數是513人之間,但已有判賠超過4000萬的案例定讞,這對醫師的醫療行為產生重大影響,保守、防衛取代積極治療,醫病關係已雙輸。

苯甲酸酯類防腐劑 耐斯 符合規定

防腐劑沒標示?耐斯聲明:莎啦莎啦、嚕啦啦、澎澎都有標 2014/10/02 13:24:00生活中心/綜合報導消基會昨(1)日發佈市售沐浴乳檢測,發現高達64的產品含有防腐劑,其中「依必朗」、「澎澎」、「嚕啦啦」、「美琪」等7項沐浴乳未標明羥苯甲酸酯類防腐劑。被點名標示不實,耐斯企業發表聲明表示,所生產的三項產品與消基會敘述事實不符,產品背後皆有清楚標示,含量也在合法範圍內。消基會今年5月進行防腐劑(對羥苯甲酸酯類、甲基異噻唑啉酮、甲基氯異噻唑啉酮)、殺菌劑、甲醛(福馬林)等含量抽查;昨(1)日公佈標示不實沐浴乳,耐斯企業發表聲明表示,對羥苯甲酸酯類防腐劑,「莎啦莎啦鳶尾花香潤沐浴乳」、「嚕啦啦薰衣草溫和沐浴乳」、「澎澎綠茶多酚活力煥膚沐浴乳」三項產品背標成分都有清楚標示Parahydroxybenzoic acid ester,並無消基會所述標示不清等情事。耐斯企業指出,根據衛服部公告之「化粧品中防腐劑成份基量使用規定表」中,對羥苯甲酸酯類(Parahydroxybenzoic acid ester)使用含量管制皆符合規定,消費者可安心使用。