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PEPTIDES WORLDWIDE.

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Keytruda, RU58841 & Urocortin II

What is Keytruda ?

Detailed Product Information

Pembrolizumab is a humanized antibody used in cancer immunotherapy. This includes to treat melanoma, lung cancer, head and neck cancer, Hodgkin lymphoma, and stomach cancer. It is given by slow injection into a vein. Common side effects include itchiness, rash, cough, fever, nausea, and constipation

Keytruda (pembrolizumab) is a medication used for the treatment of advanced melanoma, metastatic nonsquamous NSCLC, recurrent or metastatic Head and Neck Squamous Cell Carcinoma (HNSCC), recurrent classical Hodgkin Lymphoma (cHL), locally advanced or metastatic urothelial carcinoma, solid tumours having the biomarkers MSI-H or dMMR, recurrent locally advanced or metastatic gastric or gastroesophageal junction adenocarcinoma.

A decade ago, the US pharmaceuticals company Merck paid $41bn to acquire Schering-Plough, consolidating and cutting thousands of jobs amid an industry crisis of innovation and confidence. The companies touted their cholesterol and HIV treatments, briefly noting a “promising pipeline” in oncology.

Hidden in that pipeline was Keytruda, an antibody that enables the body’s immune system to attack cancers. It was an accidental acquisition, initially ignored by Merck and almost discarded but now its main blockbuster, with sales expected by JPMorgan to hit $16bn a year by the mid-2020s. It extends patients’ lives longer than chemotherapy alone, albeit expensively. Rapid innovation in oncology drugs such as Keytruda and genetic medicine has prompted another merger wave. Bristol-Myers Squibb agreed to acquire Celgene for $90bn in January, GlaxoSmithKline agreed to buy the US biotech Tesaro for $5.1bn in December, and Eli Lilly said last month it was acquiring Loxo Oncology for $8bn.

It is an exciting time for an industry that for many years struggled to make research and development produce results. It is also a welcome shift away from the mass marketing of primary care pills towards medicines for the gravely ill. This week, Keytruda was found to improve the health of patients with kidney cancer and with glioblastoma, an aggressive brain tumour. But it begs questions about the future of pharma companies. One is whether they are more innovative than before, despite this activity. The second is how long the buzz about cutting-edge oncology can convince insurers and healthcare systems to pay bills that are already high and may rise higher.

Keytruda illustrates how the industry now works — it was discovered by a Dutch pharma company that Schering-Plough bought in 2007, rather than in one of either group’s research laboratories. Merck’s role, when it finally realised what it was sitting on (thanks to seeing Bristol-Myers nurturing a rival drug called Opdivo) was to put Keytruda through trials and develop it. Keytruda and Opdivo are enormously important drugs in the developing field of cancer immunotherapy. They are “checkpoint inhibitors” that prevent the body blocking an immune response to cancer cells. Since Keytruda’s first approval in the US in 2014, it has been used to treat an expanding range of cancers, sometimes alone but often combined with other drugs. This success has pushed other pharma companies to acquire biotechs, or to form partnerships to develop similar drugs, and others that can be used with them.

A lot of drug discovery is done in biotech start-ups — the consultancy McKinsey estimates that 69 per cent of the portfolios of high-growth pharma companies came from acquisitions or licensing in 2015. That avoids the risk of working for years on a drug that fails, but it creates other challenges. A pharma group that in effect outsources early stage research can suffer from a brain drain — it may lack scientists who can assess properly which deals to strike with biotechs. It can also struggle to make the most of the drugs it acquires from others by widening their applications. This way of running the industry inflates prices. Biotech drug discovery is a risky endeavour, so investors (and research scientists who leave safe jobs) want to be rewarded richly for success.

The wave of oncology innovations encourages the fear of missing out among drugmakers — recent deals show how high a price they will pay to secure their future. In the end, the patient pays. In November, Keytruda was approved for use in the UK’s National Health Service. The list price for each three-weekly infusion is £5,260, and the average cost for a course of treatment is £84,000, although the NHS gets a discount. The official price for Kymriah, a personalised leukaemia drug from Novartis, is £282,000 per treatment. Innovative drugs are not only expensive to develop but difficult to spurn. An oncologist may have one chance to save a patient’s life and will pick the medicine with the best shot. That curbs the pressure to cut prices, in contrast with pills with generic competition or, for example, a hepatitis C drug with a rival that might also be effective. In some ways, the market is working — such is the ferment of innovation stimulated by these rewards that rivals for drugs such as Keytruda are popping up faster than before.

If cancer were less complex, one could expect prices to start falling; US President Donald Trump’s campaign against “the injustice of high drug prices” paid by Medicare would produce results. But we are decades away from anything like a “cure for cancer” and one medicine is rarely enough — many pharma groups are working on drugs for use in combination with Keytruda or Opdivo. Not only will this make splitting the rewards difficult but the overall price will rise rather than fall. It is hard to deny any patient an extra year of life but the bill will be fearsome. For now, the industry is enjoying a burst of profitability and dealmaking, with high prices justified by life-saving innovation. It knows one thing from history: the halo will fade.

What is RU58841 ?

Detailed Product Information

RU-58841, also known as PSK-3841 or HMR-3841, is a nonsteroidal antiandrogen which was formerly under investigation by ProStrakan for potential use as a topical treatment for androgen-dependent conditions including acne, pattern hair loss, and excessive hair growth. RU58841 is a specific androgen receptor antagonist or a so called anti-androgen. This non steroidal topical androgen antagonist was investigated for therapeutic value in androgenetic alopecia and acne. In studies and clinical trials RU58841 has shown to;

Strongly compete against DHT Increase cellular replication rate in the matrix cells Increase cellular proliferation of outer root sheeth cells Increase hair diameter and hair density Increase the percentage of hair in the anagen phase Exert no negative effect on body hormone levels Provide equivalent or better net growth than Finasteride

RU58841 works by binding to the androgen receptor in the hair follicle. Therefore androgens don’t have the chance to bind and start the chain reaction of androgenetic alopecia and begin the so called miniaturization process. It has been demonstrated to interrupt this hair loss message locally so that normal hair growth could continue.

What is Urocortin II ?

Detailed Product Information

Urocortin II (Ucn 2), also known as stresscopin-related peptide, is a novel predicted neuropeptide related to corticotropin-releasing factor (CRF). The peptide consisting of 38 amino acid residues was first demonstrated to be expressed centrally and to bind selectively to type 2 CRF receptor (CRFR2). In the rodent, Ucn 2 transcripts were shown to be expressed in the discrete regions of the central nervous system including stress-related cell groups in the hypothalamus and brainstem. More recently, the expression of Ucn 2 transcripts was detected in the olfactory bulb, pituitary, cortex, hypothalamus, and spinal cord. Ucn 2 mRNA was also found to be expressed widely in a variety of peripheral tissues, most highly in the skin and skeletal muscle tissues. Ucn 2-like immunoreactivity was detected by RIA in acid extracts of mouse brain, muscle, and skin. Immunohistochemically Ucn 2 was found in both skin epidermis and adnexal structures and in the skeletal muscle myocytes. Ucn 2 gene transcription was stimulated in the hypothalamus and brainstem by glucocorticoid administration to the mouse and inhibited by removal of glucocorticoids by adrenalectomy, suggesting a putative link between the CRFR1 and CRFR2 pathways.

On the other hand, in the rat a stressor-specific regulation of Ucn 2 mRNA expression in the hypothalamic paraventricular nucleus was demonstrated, which raised the possibility of a modulary role of Ucn 2 mRNA in stress-induced alteration of anterior and posterior pituitary function, depending on the type of stress. Administration of dexamethasone to the mouse resulted in a decrease of Ucn 2 mRNA levels in the back skin region. Adrenalectomy signifcantly increased Ucn 2 mRNA levels in the skin, and the levels were reduced back to normal levels after corticoid replacement. CRFR2 is found in cardiomyocytes and in endothelial and smooth muscle cells of the systemic vasculature. Ucn 2 is expressed in the mouse cardiomyocytes. In the mouse, Ucn 2 treatment augmented heart rate, exhibited potent inotropic and lusitropic actions on the left ventricle, and induced a downward shift of the diastolic pressure-volume relation. Ucn 2 also reduced systemic arterial pressure, associated with a lowering of systemic arterial elastance and systemic vascular resistance. The effects of Ucn 2 were specific to CRFR2 function and independent of beta-adrenergic receptors. These experiments demonstrated the potent cardiovascular physiologic actions of Ucn 2 in the both wild-type and cardiomyopathic mice and support a potential beneficial use of Ucn 2 in congestive heart failure treatment. The use of Ucn 2 was also proposed to treat ischemic heart disease because of its potent cardioprotective effect in the mouse heart and its minimal impact on the hypothalamic stress axis.

Administration of Ucn 2 to the mouse prevented the loss of skeletal muscle mass resulting from disuse due to casting, corticosteroid treatment, and nerve damage. In addition, Ucn 2 treatment prevented the loss of skeletal muscle force and myocyte cross-sectional area that accompanied muscle mass losses resulting from disuse due to casting. In normal muscles of the mouse, Ucn 2 increased skeletal muscle mass and force. It was thus proposed that Ucn 2 might find utility in the treatment of skeletal muscle wasting diseases including age-related muscle loss or sarcopenia. Mouse urocortin 2 (Ucn 2) is a new peptide predicted from mouse cDNA sequence and its physiologic and pathophysiologic significance has not yet been fully elucidated. However, the experimental data presented to date provided evidence for the important physiologic roles of Ucn 2 and urge the necessity of further investigation of the peptide from various points of view.

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