cythioate 115-93-5

Cythioate is an organothiophosphate chemical used as an insecticide and anthelmintic. It has been sold under the trade names Cyflee andProban, under which form it has been used for veterinary purposes against fleas

Cythioate[1][2]
Identifiers
CAS number 115-93-5 Yes
PubChem 8293
ChemSpider 7992 Yes
UNII 3OOH7Q4333 Yes
EC number 204-115-9
KEGG D07768 Yes
MeSH Cythioate
Beilstein Reference 2148114
Jmol-3D images Image 1

70978-54-0 5′-BROMO-2′-HYDROXY-3′-NITROACETOPHENONE

【Name】5′-BROMO-2′-HYDROXY-3′-NITROACETOPHENONE
【CAS】70978-54-0

【Synonyms】1-(5-BROMO-2-HYDROXY-3-NITROPHENYL)ETHANONE
3-BROMO-6-HYDROXY-5-NITRO ACETOPHENONE
5′-BROMO-2′-HYDROXY-3′-NITROACETOPHENONE
5-BROMO-2-HYDROXY-3-NITROACETOPHENONE
5′-Bromo-3′-nitro-2′-hydroxyacetophenone
【Molecular Formula】C8H6BrNO4
【MDL Number】MFCD01631134
【Molecular Weight】260.04
【MOL File】70978-54-0.mol

36445-84-8 Sodium alpha-hydroxyacrylate polymer

dentification of 36445-84-8

  • Name:Sodium alpha-hydroxyacrylate polymer (Related Reference)
  • Molecular Formula:C11H27NSi
  • CAS Registry Number:36445-84-8
  • Synonyms:2-Propenoic acid, 2-hydroxy-, monosodium salt, homopolymer;Sodium .alpha.-hydroxyacrylate polymer
  • InChI:InChI=1S/C11H27NSi/c1-4-9-13(6-3,10-5-2)11-7-8-12/h4-12H2,1-3H3

Chemical Properties

  • Molecular Weight:0009

1,8-dibromonaphthalene 17135-74-9

1,8-Dibromonaphthalene

Cas No.17135-74-9

Purity:98%up

Appearance: Buff to off-white crystal solid

Properties Computed from Structure]

Molecular Weight 285.96264 [g/mol]
Molecular Formula C10H6Br2
XLogP 4.9
H-Bond Donor 0
H-Bond Acceptor 0
Rotatable Bond Count 0
Exact Mass 285.881579
MonoIsotopic Mass 283.883625
Topological Polar Surface Area 0
Heavy Atom Count 12
Formal Charge 0
Complexity 142
Isotope Atom Count 0
Defined Atom StereoCenter Count 0
Undefined Atom StereoCenter Count 0
Defined Bond StereoCenter Count 0
Undefined Bond StereoCenter Count 0
Covalently-Bonded Unit Count 1

4-Bromotriphenylamine 36809-26-4

Name  4-Bromotriphenylamine
Synonyms  4-Bromo-N,N-diphenylaniline

Molecular Structure
4-Bromotriphenylamine, 4-Bromo-N,N-diphenylaniline, CAS #: 36809-26-4
Molecular Formula  C18H14BrN
Molecular Weight  324.21
CAS Registry Number  36809-26-4

Properties

Melting point  108-112 ºC

Safety Data

Hazard Symbols     Xn    Details
Risk Codes  R22;R36/37/38;R43
Safety Description  S26;S36/37

What is the OLED technology all about?

OLEDs are made from organic (carbon based) materials that emit light when electricity is applied. Because OLEDs do not require a backlight and filters (unlike LCD displays), they are more efficient, simpler to make, and much thinner. OLEDs have a great picture quality – brilliant colors, fast response rate and a wide viewing angle.

OLED materials have been discovered back in 1960, but only in the past 20 years or so have researchers started to actually work on the technology. A complete history of OLEDs can be found here. You can read more about OLED displays and advantages in our OLED introduction page.

How do OLEDs work?

The basic structure of an OLED is a cathode (which injects electrons), an emissive layer and an anode (which removes electrons). Modern OLED devices use many more layers in order to make them more efficient, but the basic functionality remains the same.

How an OLED panel is made

Making an OLED involves several steps: taking a substrate, cleaning it, making the backplane (the switching and driving circuitry), depositing and patterning the organic layers and finally encapsulation the whole thing to prevent dust, oxygen and moisture damage.

There are several ways to deposit and pattern the organic layers. Currently all OLED displays are made using vacuum evaporation, using a Shadow Mask (FMM, Fine Metal Mask) to pattern. This is a relatively simple method but it is inefficient and very difficult to scale up to large substrates. There are several alternatives for next-gen deposition techniques, including laser annealing and inkjet printing. These methods will be scalable and more efficient than vacuum deposition.

OLED materials

There are several types of OLED materials. The most basic division is between small-molecule OLEDs and large molecule ones (called Polymer OLEDs, or P-OLEDs). Almost all OLEDs made today are SM-OLED based. These materials are evaporable and far more advanced than P-OLEDs. P-OLEDs had great promise and are solution processable (and so can be used in InkJet printing and spin-coating fabrication methods). Intensive research is being performed to develop efficient solution-processable SM-OLEDs.

Another interesting division is between Fluorescent and Phosphorescent materials. Fluorescent materials last longer (and were discovered first) but are much less efficient than Phosphorescent materials. Most people agree that the future of OLEDs (especially in large-area displays and lighting panels) lie with Phosphorescent materials, although there are still challenges in developing a long-lasing blue Phosphorescent OLED. It is possible to combine these materials though, and today Samsung for example use a red PHOLED together with Fluorescent green and blue. Universal Display Corporation is pioneering PHOLED research, holding basic patents in this area.

AMOLED vs PMOLED

These terms relate to the driving method of the OLED display. A PMOLED (Passive-Matrix OLED) is limited in size and resolution, but is cheaper and easier to make than an AMOLED (which uses an Active-Matrix). An AMOLED uses an active-matrix TFT array and storage capacitors. While these displays are more efficient and can be made large, they are also more complicated to make.

PMOLED displays are used in mp3 players or secondary displays on cell phones while AMOLEDs are used in smartphone displays, digital cameras and TVs.

Challenges

The two major challenges facing the OLED industry is the lifetime of the panels (OLED panels still lag behind plasma and LCD displays) and production scaling beyond Gen-5.5.

OLED technology today

Today OLED displays are used mainly in small (2″ to 5″) displays for mobile devices such as phones, cameras and MP3 players. OLED displays carry a price premium over LCDs, but offer brighter pictures and better power efficiency – making it ideal for battery powered gadgets.

Making larger OLEDs is possible, but difficult and expensive. There are some OLED TVs available, but these are expensive. Sony has announced the XEL-1 11quot; OLED TV back in 2007 – at about $2,500 (they aren’t producing it anymore and now focus on professional OLED monitors). LG is also offering an OLED TV (the 15″EL9500) which is also expensive and isn’t being mass produced. Mass production of price-competitive OLED TV sets will probably begin towards the end of 2012 or early 2013.

In the OLED lighting market, several companies (such as Philips, OSRAM and Lumiotec) are already shipping OLED panels, but these are small and very expensive, mostly used in premium lighting fixtures and as experimental design kits.

Zidovudine 30516-87-1

Zidovudine (INN) or azidothymidine (AZT) (also called ZDV) is a nucleoside analog reverse-transcriptase inhibitor (NRTI), a type of antiretroviral drug used for the first clinically proven successful treatment of HIV/AIDS infectiousness. It is a therapeutic analog of thymidine that targets HIV exclusively. It remains in widespread use today and is recognized by the Centers for Disease Control as one of the most effective drugs in medical history.

AZT is the first U.S. government-approved treatment for HIV therapy, prescribed under the names Retrovir and Retrovis. AZT was the first breakthrough in AIDS therapy, significantly reducing the replication of the virus in patients and leading to clinical and immunologic improvements.[2] It can also be used to prevent HIV transmission, such as from mother to child during the period of birth or after a needle stick. Used by itself in HIV-infected patients, AZT safely slows HIV replication in patients, but generally does not stop it entirely.[3] This may allow HIV to become AZT-resistant over time, and for this reason AZT is usually used in conjunction with the other anti-HIV drugs in combination therapy called highly active antiretroviral therapy (HAART).

To simplify its use in combination, AZT is included in Combivir and Trizivir, among others. Zidovudine is mandated in the “Essential Drugs List” of theWorld Health Organization, which is a list of minimum medicinal needs for a basic health care system

Zidovudine
Systematic (IUPAC) name
1-[(2R,4S,5S)-4-azido-5-(hydroxymethyl)oxolan-2-yl]-5-methylpyrimidine-2,4-dione[1]
Clinical data
AHFS/Drugs.com monograph
Pregnancy cat. B3 (AU) C (US)
Legal status ℞ Prescription only
Routes Oral, Serum, Suppository
Pharmacokinetic data
Bioavailability complete absorption, following first-pass metabolism systemic availability 75% (range 52 to 75%)
Protein binding 30 to 38%
Metabolism Hepatic
Half-life 0.5 to 3 hours
Excretion Renal/Rectal
Identifiers
CAS number 30516-87-1 Yes
ATC code J05AF01
PubChem CID 35370
DrugBank DB00495
ChemSpider 32555 Yes
UNII 4B9XT59T7S Yes
ChEBI CHEBI:10111 
ChEMBL CHEMBL129 Yes
NIAID ChemDB 000002
Chemical data
Formula C10H13N5O4 
Mol. mass 267.242 g/mol

Chemistry

A salt crystal of AZT, viewed under polarized x-rays

AZT crystallizes into an asymmetric nucleated monoclinic salt structure, forming an equalized hydrogen-nitrogen-oxygen bonded protease network of triple base-paired excimer dimers; its multiscaled crystallized lattice superstructure and surfactant headgroup electrostatic bond polarity was reported in 1988 and 1987.[5][6]

[edit]History

[edit]Development

In the 1960s the theory that most cancers were caused by environmental retroviruses gained clinical support and funding. It had recently become known, due to the work of Nobel laureates Howard Temin and David Baltimore,[7] that nearly all avian cancers were caused by bird retroviruses, but corresponding human retroviruses were not known yet.

In parallel work, other compounds that successfully blocked the synthesis of nucleic acids had been proven to be both antibacterial, antiviral, and anticancer agents, the leading work being done at the laboratory of Nobel laureates George Hitchings and Gertrude Elion, leading to the development of the antitumor agent 6-mercaptopurine.[7]

Jerome Horwitz of the Barbara Ann Karmanos Cancer Institute and Wayne State University School of Medicine first synthesized AZT in 1964 under aUS National Institutes of Health (NIH) grant.[8][9][10] Development was shelved after it proved biologically inert in mice.[8][11] In 1974, Wolfram Ostertag of the Max Planck Institute in Germany reported that AZT specifically targeted Friend virus (strain of murine leukemia virus).[12]

[edit]Successful HIV Treatment

In May 1984, shortly after the human immunodeficiency virus (HIV) had been unambiguously proved as the cause of AIDS, Samuel Broder, Hiroaki Mitsuya, and Robert Yarchoan of the United States National Cancer Institute (NCI) initiated a program to develop therapies for HIV/AIDS.[13]Using a CD4+ cell line that they had made, they developed an assay to screen drugs for their ability to protect CD4+ T cells from being killed by HIV.[14] This assay could simultaneously test both the anti-HIV effect of the compounds and their toxicity against infected T cells. In order to get drugs into the clinic as soon as possible, they started with compounds that were either in clinical use or for which they could get a pharmaceutical partner. As part of this effort, they initiated a collaboration with scientists at the Burroughs-Wellcome Company (now GlaxoSmithKline). Burroughs-Wellcome had expertise in nucleoside analogs and viral diseases, led by researchers including Gertrude Elion, David Barry, Paul (Chip) McGuirt Jr., Philip Furman, Martha St. Clair, Janet Rideout, Sandra Lehrman and others. Their research efforts were focused in part on the viral enzymereverse transcriptase. Reverse transcriptase is an enzyme that retroviruses, including HIV, utilize to replicate themselves. One compound that they were working with (AZT), which they had given the code name “BW A509X”, was tested and demonstrated remarkable efficacy against certain mouse viruses. However, the scientists at Burroughs-Wellcome were not working with HIV themselves, and sent 11 compounds to the NCI team for testing against HIV in their newly developed assay. In February 1985, the NCI scientists found that BW A509X, one of these compounds, had potent efficacy in vitro and in rodents.[8][14] Several months later, Broder, Mitsuya, and Yarchoan started the initial phase 1 clinical trial of AZT at the NCI, in collaboration with the scientists from Burroughs-Wellcome and Duke University.[15][16] In doing this Phase I trial, they built on their experience in doing an earlier trial, with suramin, another drug that had shown effective anti-HIV activity in the laboratory. This initial trial of AZT proved that the drug could be safely administered to patients with HIV, that it increased their CD4 counts, restored T cell immunity as measured by skin testing, and that it showed strong evidence of clinical effectiveness, such as inducing weight gain in AIDS patients. It also showed that levels of AZT that worked in the test tube could be injected into patients in serum and suppository form, and that the drug penetrated deeply only into infected brains.

A rigorously maintained double-blind, placebo-controlled randomized trial of AZT was subsequently conducted by Burroughs-Wellcome. The study, which was commended by the CDC and the NIH for its standards,[17] proved that AZT safely prolongs the lives of patients with HIV.[18] Burroughs-Wellcome filed for a patent for AZT in 1985. The United States Food and Drug Administration (FDA) approved the drug (via the then-new FDA accelerated approval system) for use against HIV, AIDS, and AIDS Related Complex (ARC, a now-obsolete medical term for pre-AIDS illness) on March 20, 1987.[19] The time between the first demonstration that AZT was active against HIV in the laboratory and its approval was 25 months, the shortest period of drug development in recent history.

AZT was subsequently approved unanimously for infants and children in 1990.[20] AZT was initially administered in somewhat higher dosages than today, typically 400 mg every four hours, day and night. The paucity of alternatives for treating HIV/AIDS at that time unambiguously affirmed the health risk/benefit ratio, with inevitable slow, disfiguring, and painful death from HIV outweighing the drug’s side-effect such as anemia and malaise.

Current treatment regimens involve relatively lower dosages (e.g., 300 mg) of AZT taken just twice a day, almost always as part of highly active antiretroviral therapy (HAART), in which AZT is combined with other drugs (known affectionately as “the triple cocktail”) in order to prevent the mutation of HIV into an AZT-resistant form. [21][22]

HIV Prophylaxis

AZT is used as post-exposure prophylaxis in combination with another antiretroviral, Lamivudine, substantially reducing the risk of HIV infection following the first single exposure to the virus (such as a needle-stick injury involving blood or body fluids from an individual known or suspected of being infected with HIV).[23]

AZT is now a principal part of the clinical pathway for both pre-exposure prophylaxis and post-exposure treatment of mother-to-child transmission of HIV during pregnancy, labor, and delivery and has been proven to be integral to uninfected siblings’ perinatal and neonatal development.[24][25] Without AZT, as many as 10 to 15% of fetuses with HIV-infected mothers will themselves become infected.[26] AZT has been shown to reduce this risk to as little as 8% when given in a three-part regimen post-conception, delivery, and six weeks post-delivery. Consistent and proactive precautionary measures, such as the rigorous use of antiretroviral medications, cesarean section, face masks, heavy-duty rubber gloves, clinically-segregated disposable diapers, and avoidance of mouth contact and breast feeding will further reduce child-attendant transmission of HIV to as little as 1–2%.[27][28][29] However, a new study now indicates that HIV+ mothers not taking antiretrovirals who breastfeed their children will help prevent HIV transmission to their infants.[30]

During the period from 1994 to 1999 when this was the primary form of prevention of mother-to-child HIV transmission, AZT prophylaxis prevented more than 1000 parental and infant deaths from AIDS in the United States.[31]

Side effects

AZT-based antiretroviral therapy has been proven to significantly reduce rates of certain AIDS-defining cancers (most dramatically, that of Kaposi’s sarcoma and central nervous system lymphoma).[32][33][34]

Early long-term higher-dose therapy with AZT was initially associated with side effects that sometimes limited therapy, including anemia, neutropenia, hepatotoxicity, cardiomyopathy, andmyopathy. All of these conditions were generally found to be reversible upon reduction of AZT dosages. They have been attributed to several possible causes, including transient depletion ofmitochondrial DNA, sensitivity of the γ-DNA polymerase in some cell mitochondria,[35] the depletion of thymidine triphosphate, oxidative stress, reduction of intracellular L-carnitine orapoptosis of the muscle cells.[36] Anemia due to AZT was successfully treated using vitamins to stimulate red blood cell production.[37][38] Drugs that inhibit hepatic glucuronidation, such asindomethacin, nordazepam, acetylsalicylic acid (aspirin) and trimethoprim, decreased the elimination rate and increased the therapeutic strength of the medication.[39] Most common side-effects included upset stomach and acid reflux (heartburn), headache, cosmetic reduction in abdominal body fat, light sleeping, and occasional loss of appetite; while less-common complaints included faint discoloration of fingernails and toenails, mood elevation, occasional tingling or transient numbness of the hands or feet, and minor skin discoloration. Allergic reactions were rare.[40] Today, side-effects are much less common with the use of lower doses of AZT.[41] According to IARC, there is sufficient evidence in experimental animals for the carcinogenicity of zidovudine; it is possibly carcinogenic to humans (Group 2B).[42]

[edit]Viral resistance

Even at the highest doses that can be tolerated in patients, AZT is not potent enough to prevent all HIV replication, and may only slow the replication of the virus and the progression of the disease. During prolonged AZT treatment, HIV has the potential to develop resistance to AZT by mutation of its reverse transcriptase.[43][44] To slow the development of resistance, physicians generally recommend that AZT be given in combination with another reverse transcriptase inhibitor and an antiretroviral from another group, such as a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor; this type of therapy is known as HAART (Highly Active Anti Retroviral Therapy). AZT has been shown to work additively or synergistically with many antiviral agents such as acyclovir and interferon; however, ribavirin decreases the antiviral effect of AZT.[citation needed]

[edit]Mechanism of action

AZT in oral, injectable, and suppository form

AZT works by selectively inhibiting HIV’s reverse transcriptase, the enzyme that the virus uses to make a DNA copy of its RNA. Reverse transcription is necessary for production of HIV’s double-stranded DNA, which would be subsequently integrated into the genetic material of the infected cell(where it is called a provirus).[45][14][16]

The azido group increases the lipophilic nature of AZT, allowing it to cross infected cell membranes easily by diffusion and thereby also to cross the blood–brain barrier. Cellular enzymes convert AZT into the effective 5′-triphosphate form. Studies have proven that the termination of HIV’s forming DNA chains is the specific factor in the inhibitory effect.

At very high doses, AZT’s triphosphate form may also inhibit DNA polymerase used by human cells to undergo cell division, but regardless of dosage AZT has an approximately 100-fold greater affinity for HIV’s reverse transcriptase.[46] The selectivity has been proven to be due to the cell’s ability to quickly repair its own DNA chain if it is broken by AZT during its formation, whereas the HIV virus lacks that ability.[47] Thus AZT inhibits HIV replication without affecting the function of uninfected cells.[14] At sufficiently high dosages, AZT begins to inhibit the cellular DNA polymerase used by mitochondria to replicate, accounting for its potentially toxic but reversible effects on cardiac and skeletal muscles, causingmyositis.[48][49][50][51][15]

AZT’s therapeutic mechanism is unrelated to chemotherapy and cannot negatively impact the immune system.[52]

Patent issues

The patents on AZT have been the target of some controversy. In 1991, Public Citizen filed a lawsuit claiming that the patents were invalid. Subsequently, Barr Laboratories and Novopharm Ltd. also challenged the patent, in part based on the assertion that NCI scientists Samuel Broder, Hiroaki Mitsuya, and Robert Yarchoan should have been named as inventors, and those two companies applied to the FDA to sell AZT as a generic drug. In response, Burroughs Wellcome Co. filed a lawsuit against the two companies. The United States Court of Appeals for the Federal Circuit ruled in 1992 in favor of Burroughs Wellcome, claiming that even though they had never tested it against HIV, they had conceived of it working before they sent it to the NCI scientists.[53] This suit was appealed up to the Supreme Court of the US, but they declined to formally review it. In 2002, another lawsuit was filed over the patent by the AIDS Healthcare Foundation.

However, the patent expired in 2005 (placing AZT in the public domain), allowing other drug companies to manufacture and market generic AZT without having to pay GlaxoSmithKline any royalties. The U.S. FDA has since approved four generic forms of AZT for sale in the U.S.

In November 2009 GlaxoSmithKline formed a joint venture with Pfizer which combined the two companies’ HIV assets in one company called ViiV Healthcare. This included the rights to Zidovudine.

Uridine triphosphate 63-39-8

Uridine-5′-triphosphate (UTP) is a pyrimidine nucleoside triphosphate, consisting of the organic base uracil linked to the 1′ carbon of the ribosesugar, and esterified with tri-phosphoric acid at the 5′ position. Its main role is as substrate for the synthesis of RNA during transcription.

Uridine triphosphate
Identifiers
CAS number 63-39-8 Yes
PubChem 1181
MeSH Uridine+triphosphate
ChEMBL CHEMBL605653 
Properties
Molecular formula C9H15N2O15P3
Molar mass 484.141

Role in metabolism

UTP also has the role of a source of energy or an activator of substrates in metabolic reactions, like that of ATP, but more specific. When UTP activates a substrate, UDP-substrate is usually formed and inorganic phosphate is released. UDP-glucose enters the synthesis of glycogen. UTP is used in the metabolism of galactose, where the activated form UDP-galactose is converted to UDP-glucose. UDP-glucuronate is used to conjugate bilirubin to a more water-soluble bilirubin diglucuronide.

Role in receptor mediation

UTP also has roles in mediating responses by extracellular binding to the P2Y receptors of cells. UTP and its derivatives are still being investigated for their applications in human medicine.