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DR ANTHONY MELVIN CRASTO, WORLDDRUGTRACKER

Novartis’ Breakthrough Therapy For A Rare Muscle-Wasting Disease

 drugs  Comments Off on Novartis’ Breakthrough Therapy For A Rare Muscle-Wasting Disease
Sep 162013
 

 

 

On August 20, 2013, Novartis announced in a press release that the FDA had granted breakthrough therapy designation to its experimental agent BYM338 (bimagrumab) for treatment of the rare muscle wasting disease sporadic inclusion body myositis (sIBM).

sIBM is a rare–but increasingly prevalent–disease. It is the most common cause of inflammatory myopathy in people over 50. sIBM has a yearly incidence of 2 to 5 per million adults with a peak at ages 50 to 70, with male predominance. Muscle wasting caused by sIBM is superimposed upon the sarcopenia (degenerative loss of muscle mass) that typically occurs with aging.

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http://biopharmconsortium.com/blog/2013/09/04/novartis-breakthrough-therapy-rare-muscle-wasting-disease/

 

bimagrumab

immunoglobulin G1-lambda2, anti-[Homo sapiens ACVR2B (activin
A receptor type IIB, ActR-IIB)], Homo sapiens monoclonal antibody;
gamma1 heavy chain (1-445) [Homo sapiens VH (IGHV1-2*02
(91.80%) -(IGHD)-IGHJ5*01 [8.8.8] (1-115) -IGHG1*03 (CH1 (116-
213), hinge (214-228), CH2 L1.3>A (232), L1.2>A (233) (229-338),
CH3 (339-443), CHS (444-445)) (116-445)], (218-216′)-disulfide with
lambda light chain (1′-217′) [Homo sapiens V-LAMBDA (IGLV2-
23*02 (90.90%) -IGLJ2*01) [9.3.11] (1′-111′) -IGLC2*01 (112′-217′)];
dimer (224-224”:227-227”)-bisdisulfide
myostatin inhibitor
bimagrumab immunoglobuline G1-lambda2, anti-[Homo sapiens ACVR2B
(récepteur type IIB de l’activine A, ActR-IIB)], Homo sapiens
anticorps monoclonal;
chaîne lourde gamma1 (1-445) [Homo sapiens VH (IGHV1-2*02
(91.80%) -(IGHD)-IGHJ5*01 [8.8.8] (1-115) -IGHG1*03 (CH1 (116-
213), charnière (214-228), CH2 L1.3>A (232), L1.2>A (233) (229-
338), CH3 (339-443), CHS (444-445)) (116-445)], (218-216′)-
disulfure avec la chaîne légère lambda (1′-217′) [Homo sapiens
V-LAMBDA (IGLV2-23*02 (90.90%) -IGLJ2*01) [9.3.11] (1′-111′) –
IGLC2*01 (112′-217′)]; dimère (224-224”:227-227”)-bisdisulfure
inhibiteur de la myostatine

inmunoglobulina G1-lambda2, anti-[Homo sapiens ACVR2B
(receptor tipo IIB de la activina A, ActR-IIB)], anticuerpo monoclonal
de Homo sapiens;
cadena pesada gamma1 (1-445) [Homo sapiens VH (IGHV1-2*02
(91.80%) -(IGHD)-IGHJ5*01 [8.8.8] (1-115) -IGHG1*03 (CH1 (116-
213), bisagra (214-228), CH2 L1.3>A (232), L1.2>A (233) (229-338),
CH3 (339-443), CHS (444-445)) (116-445)], (218-216′)-disulfuro con
la cadena ligera lambda (1′-217′) [Homo sapiens V-LAMBDA
(IGLV2-23*02 (90.90%) -IGLJ2*01) [9.3.11] (1′-111′) -IGLC2*01
(112′-217′)]; dímero (224-224”:227-227”)-bisdisulfuro
inhibidor de la miostatina
1356922-05-8

Heavy chain / Chaîne lourde / Cadena pesada
QVQLVQSGAE VKKPGASVKV SCKASGYTFT SSYINWVRQA PGQGLEWMGT 50
INPVSGSTSY AQKFQGRVTM TRDTSISTAY MELSRLRSDD TAVYYCARGG 100
WFDYWGQGTL VTVSSASTKG PSVFPLAPSS KSTSGGTAAL GCLVKDYFPE 150
PVTVSWNSGA LTSGVHTFPA VLQSSGLYSL SSVVTVPSSS LGTQTYICNV 200
NHKPSNTKVD KRVEPKSCDK THTCPPCPAP EAAGGPSVFL FPPKPKDTLM 250
ISRTPEVTCV VVDVSHEDPE VKFNWYVDGV EVHNAKTKPR EEQYNSTYRV 300
VSVLTVLHQD WLNGKEYKCK VSNKALPAPI EKTISKAKGQ PREPQVYTLP 350
PSREEMTKNQ VSLTCLVKGF YPSDIAVEWE SNGQPENNYK TTPPVLDSDG 400
SFFLYSKLTV DKSRWQQGNV FSCSVMHEAL HNHYTQKSLS LSPGK 445
Light chain / Chaîne légère / Cadena ligera
QSALTQPASV SGSPGQSITI SCTGTSSDVG SYNYVNWYQQ HPGKAPKLMI 50
YGVSKRPSGV SNRFSGSKSG NTASLTISGL QAEDEADYYC GTFAGGSYYG 100
VFGGGTKLTV LGQPKAAPSV TLFPPSSEEL QANKATLVCL ISDFYPGAVT 150
VAWKADSSPV KAGVETTTPS KQSNNKYAAS SYLSLTPEQW KSHRSYSCQV 200
THEGSTVEKT VAPTECS 217
Disulfide bridges location / Position des ponts disulfure / Posiciones de los puentes disulfuro
Intra-H 22-96 142-198 259-319 365-423
22”-96” 142”-198” 259”-319” 365”-423”
Intra-L 22′-90′ 139′-198′
22”’-90”’ 139”’-198”’
Inter-H-L 218-216′ 218”-216”’
Inter-H-H 224-224” 227-227”
N-glycosylation sites / Sites de N-glycosylation / Posiciones de N-glicosilación
H CH2 N84.4

Bimagrumab

http://www.who.int/medicines/publications/druginformation/innlists/PL108_Final.pdf

Novartis announced that the US Food and Drug Administration (FDA) has granted breakthrough therapy designation to BYM338 for sporadic inclusion body myositis (sIBM). This designation is based on the results of a phase 2 proof-of-concept study that showed BYM338 substantially benefited patients with sIBM compared to placebo.

read all at

http://www.dddmag.com/news/2013/08/novartis-muscle-drug-gets-breakthrough-status?et_cid=3433957&et_rid=523035093&type=headline

Novartis receives FDA breakthrough therapy designation for BYM338 (bimagrumab) for sporadic inclusion body myositis (sIBM)

•    Designation highlights potential of BYM338 to address an unmet medical need in a serious disease
•    If approved, BYM338 has the potential to be the first treatment for sIBM patients
•    BYM338 is the third Novartis investigational treatment this year to receive a breakthrough therapy designation by the FDA, highlighting Novartis’ leadership in the industry in breakthrough therapy designations

Bimagrumab (BYM338) is a human monoclonal antibody developed by Novartis to treat pathological muscle loss and weakness. On August 20, 2013 it was announced that bimagrumab was granted breakthrough therapy designation for sporadic inclusion body myositis(sIBM) by US Food and Drug Administration.[1]

 

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LEVOCETRIZINE

 drugs  Comments Off on LEVOCETRIZINE
Sep 152013
 

File:Levocetirizine structure 2.svg
LEVOCETRIZINE

Levocetirizine (as levocetirizine dihydrochloride) is a third-generation non-sedative antihistamine, developed from the second-generation antihistamine cetirizine. Chemically, levocetirizine is the active enantiomer of cetirizine. It is the R-enantiomer of the cetirizine racemate. Levocetirizine works by blocking histamine receptors. It does not prevent the actual release of histamine from mast cells, but prevents it binding to its receptors. This in turn prevents the release of other allergy chemicals and increased blood supply to the area, and provides relief from the typical symptoms of hay fever.
The manufacturers claim it to be more effective with fewer side effects than the second-generation drugs; however, there have been no published studies supporting this assertion, although other studies have concluded it may be more effective.[1]

History and formulations

Levocetirizine was first launched in 2001 by Belgian pharmaceutical company UCB. It is sold under the brand name Xyzal/ˈzaɪzæl/ in Australia, Czech Republic, Austria, Finland, France, Ireland, Netherlands, Portugal, Romania, Taiwan, Turkey, United States, South Africa and UK; Xuzal in Mexico; Xusal in Germany; and Xozal in Greece. In Hungary it is marketed by Richter Gedeon under the Zilola brand name.

In India, levocetirizine is marketed by GlaxoSmithKline under the brand name Vozet and Xyzal. On May 25, 2007, theUnited States Food and Drug Administration approved Xyzal, where it is co-marketed by Sanofi-Aventis. Torrent Pharma launched UVNIL in rural market of India. It is also available as LEZYNCET 5 mg tablets through Unichem in India. In India, generic name of Lev-Cit 5 mg is manufactured by VIP Pharmaceuticals. Also marketed in India by Croslands (Ranbaxy Laboratories Ltd.) under the brand name Teczine. In Brazil it is marketed under the brand name ‘Zyxem’ by Farmalab. It is marketed in Egypt by BORG Pharma under the brand name ‘Xaltec’, Allear by western pharmaceuticals and levcet by marcryl.
In Pakistan levocetirizine was first launched in liquid formulation by Novartis Consumer Health Division by the name of T-Day Syrup. It is available as 5 mg-strength tablets and a 0.5 mg/mL oral solution. In Pakistan levocetirizine is available in liquid formulation as well with the name of OCITRA and T-Day 2.5 mg/5 mL. In Bangladesh levocetirizine is available in 5 mg tablet & 2.5 mg/5 mL oral liquid formulation with the brand name of Alcet marketed by Healthcare Pharmaceuticals and Seasonix marketed by Incepta Pharmaceuticals. In Nepal levocetirizine is available in 5 mg tablet with brand name ofCurin manufactured by Beximco Pharma.[2]

Side effects

levocetirizine is called a non-sedating antihistamine as it does not enter the brain in significant amounts, and is therefore unlikely to cause drowsiness. However, some people may experience some slight sleepiness, headache, mouth dryness,lightheadedness, vision problems (mainly blurred vision), palpitations and fatigue.[3]

Research

latest research shows levocetirizine reduces asthma attacks by 70% in children.[4]

Availability]

The drug is currently available by prescription in the United States. Although the drug was only authorized by the FDA on 25 May 2007, it was already available in most European countries. Like many new drugs it entered the market at a higher price than currently available third and second generation antihistamines. In India, one form of the drug is available as Crohist MK tablets and syrup, a formulation of levocetirizine hydrochloride and montelukast. In India, Crohist MK is a Schedule ‘H’ drug and may only be prescribed by a registered medical practitioner. In Finland, the drug is sold over-the-counter.

Different brands (Actavis, Glenmark, UCB) Levocetirizine tablets and oral solution.

  1. ^ Grant, JA; Riethuisen, JM; Moulaert, B; DeVos, C; Gamalero, C.; Descalzi, D.; Folli, C.; Passalacqua, G. et al. (2002-02). “A double-blind, randomized, single-dose, crossover comparison of levocetirizine with ebastine, fexofenadine, loratadine, mizolastine, and placebo: suppression of histamine-induced wheal-and-flare response during 24 hours in healthy male subjects.”. Ann Allergy Asthma Immunol 88 (2): 190–197. doi:10.1016/S1081-1206(10)61995-3. PMID 11868924.
  2. ^ http://www.beximco-pharma.com/allergic-disorders/147-curin.html
  3. ^ XOZAL technical specifications booklet.
  4. ^ Pasquali, M; Baiardini, I; Rogkakou, A; Riccio, AM; Gamalero, C; Descalzi, D; Folli, C; Passalacqua, G et al. (2006-09).“Levocetirizine in persistent allergic rhinitis and asthma: effects on symptoms, quality of life and inflammatory parameters.”.Clinical & Experimental Allergy 36 (9): 1161–7. doi:10.1111/j.1365-2222.2006.02548.x. PMID 16961716.

xyzal_structure.png
Figure 1-The chemical structure of Xyzal
BACKGROUND

Cetirizine, chemically [2-[4-[(4-chlorophenyl)phenylmethyl]-1-piperazinyl]ethoxy]acetic acid is an antihistamine non-sedating type histamine H1-receptor antagonist, indicated for relief of symptoms associated with seasonal allergic rhinitis, perennial allergic rhinitis and related diseases.
Figure US20110184174A1-20110728-C00003
U.S. Pat. No. 4,525,358 and its equivalent EP 58146 disclose cetirizine and its pharmaceutically acceptable salts. The process for the synthesis of cetirizine comprises condensation of 1-[(4-chlorophenyl)-phenylmethyl]piperazine with 2-chloroethoxy acetamide to obtain 2-[2-[4-[(4-chlorophenyl)phenylmethyl]-1-piperazinyl]-ethoxy acetamide which on hydrolysis gives cetirizine.
It was found later that the pharmacological activity resides primarily in (R)-isomer or (−) form known as levocetirizine. GB 2225321 describes a process for the preparation of the dextro and levorotatory isomers of cetirizine comprising hydrolysis of 2-[2-[4-[(4-chlorophenyl)phenylmethyl]-1-piperazynyl]-ethoxy acetonitrile.
Figure US20110184174A1-20110728-C00004
(−)-1-[(4-chlorophenyl)-phenylmethyl]piperazine is a very important intermediate in the synthesis of levocetirizine. U.S. Pat. No. 5,478,941 discloses a process for the synthesis of (−)-1-[(4-chlorophenyl)-phenylmethyl]piperazine involving hydrolyzing 1-[(4-chlorophenyl)-phenylmethyl]-4-(4-methylphenyl)sulfonyl piperazine with hydrobromic acid in the presence of 4-hydroxybenzoic acid.
Figure US20110184174A1-20110728-C00005
The alternative routes of synthesis of (−)-1-[(4-chlorophenyl)-phenylmethyl]piperazine disclosed in the prior art involve the use of bis chloro ethylamine which is carcinogenic in nature.
Levocetirizine is a highly-potent non-sedating anti-allergic agent. Hence, there are continuous attempts to develop new processes for the synthesis of levocetirizine and its intermediates. The present invention describes a new process for the preparation of the key intermediate (−)-1-[(4-chlorophenyl)-phenylmethyl]piperazine.
Levorotatory [2-[4-[(4-chlorophenyl)phenylmethyl]-1-piperazinyl]ethoxy]acetic acid, also known by the generic name of levocetirizine, has proven useful as a therapeutic agent for the treatment of allergic disease.
Levocetirizine and its salts including its dihydrochloride are known and are effective in the treatment of allergies, including but not limited to, chronic and acute allergic rhinitis, allergic conjunctivitis, pruritus, urticaria and the like. Levocetirizine belongs to the second generation of H1 histamine receptor antagonists, which are believed to offer significant advantages over first generation compounds. Studies have shown that levocetirizine provides safe and effective symptomatic relief of seasonal allergies. Levocetirizine is used also for treating chronic idiopathic urticaria.
GB 2,225,321 describes a process for the preparation of cetirizine in the levorotatory form, dextrorotatory form or a mixture thereof comprising the hydrolysis of enantiomerically pure [2-[4-[(4-chlorophenyl)phenylmethyl]-1-piperazinyl]ethoxy]acetonitrile. Hydrolysis takes place in aqueous, alcoholic or aqueous-alcoholic medium by a base or by an acid; the acid thus obtained is converted to its dihydrochloride. Optically active starting material 1-[(4-chlorophenyl)phenylmethyl]piperazine is obtained by resolution of the corresponding racemic compound, preferably by conversion to its diastereoisomeric salt with tartaric acid. The yield of resolution is rather low, namely only 12.7%. The obtained optically active intermediate is further converted with chloroethoxyacetonitrile in 69% yield.
EP 0 617 028 and EP 0 955 295 disclose a process for the preparation of optically active 1-[(4-chlorophenyl)phenylmethyl]piperazine and its conversion to cetirizine in the levorotatory form or dextrorotatory form or to derivative thereof. The process for the preparation is shown in the following scheme:
Figure US08049011-20111101-C00001
The drawback of the disclosed reaction is that it requires protection of N,N-bis(2-haloethyl)amine, and consequently deprotection of the intermediate obtained.
Preparation of Cetirizine in its Levorotatory Form Proceeds in most known syntheses from enantiomerically pure 1-[(4-chlorophenyl)phenylmethyl]piperazine. Consequently it appears to be very desirable to provide new routes to prepare the enantiomers thereof with improved optical purity and good yields.
Polymorphic form I of crystalline levorotatory dihydrochloride salt of cetirizine and amorphous form thereof are disclosed in WO 2004/050647 and WO 2004/065360. Crystalline form is prepared by crystallization from ketone-containing solvent, such as acetone, methyl ethyl ketone, dimethylketone, 2-pentanone and mixtures thereof. Amorphous form was prepared by solvent evaporation.
There still exists a need for an efficient synthesis of levocetirizine, new intermediates used in the process, suitable for large-scale production.
Synthesis of Xyzal:
Figure 2 displays the synthesis of Cetirizine (Zyrtec). Levocetirizine, the R-enantiomer of cetirizine, is then formed from pyroglutamate salts in a synthesis that does not have attainable details.

REAL_ceterizine_synthesis.png
(Figure 2)

The synthesis of Cetrizine begins by reducing molecule 33 with a catecholborane. This reaction yields molecule 34, which is then treated with tetraflouroboric acid and reacted with an amine, compound 35. In order to remove the chromium group, the compound is refluxed in pyridine and undergoes an acid hydrolysis. This results in a yield of cetrizine.

Identification of all chirality centers:
Stereogenic centers are carbon atoms that are bonded to 4 groups. Tetrahedral stereogenic centers are stereogenic centers that are not only bonded to 4 groups but are more importantly bonded to 4 different groups. If a molecule contains 1 tetrahedral stereogenic center it is said to be chiral (nonsuperimposable on its mirror image).If a given compound contains more than 1 stereogenic center it must be further analyzed to determine if it is chiral or achiral(superimosable on its mirror image). The carbon atom bonded to the phenyl groups was found to be a tetrahedral stereogenic center. Therefore,xyzal,which was found to contain only 1 tetrahedral stereogenic center is generally considered a chiral compound because it meets the requirements of chirality and does not have a plane of symmetry that superimposes one half of the molecule on the other and is not super imposable on its mirror image.

Spectral data for Xyzal (IR and NMR):
cetirizine_IR.png
xyzal_nmr.png

 

– See more at: http://worlddrugtracker.blogspot.in/#sthash.6Ndn04WU.dpuf

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ESCITALOPRAM

 GENERIC, Uncategorized  Comments Off on ESCITALOPRAM
Sep 152013
 

File:Escitalopram structure.svg

128196-01-0 ESCITALOPRAM

Escitalopram (also known under various trade names) is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. It is approved by the U.S. Food and Drug Administration (FDA) for the treatment of adults and children over 12 years of age with major depressive disorder and generalized anxiety disorder. Escitalopram is the (S)-stereoisomer (enantiomer) of the earlier Lundbeck drug citalopram, hence the name escitalopram. Escitalopram is noted for its high selectivity with serotonin reuptake inhibition. The similarity between escitalopram and citalopram has led to accusations of “evergreening“, an accusation that Lundbeck has rejected.[1]

Escitalopram has FDA approval for the treatment of major depressive disorder and generalized anxiety disorder in adults.[2]

Off-label uses

Escitalopram is sometimes prescribed off-label for the treatment of other conditions: social anxiety disorder,[3] panic disorder[4]and obsessive-compulsive disorder.[5] There is some evidence favouring escitalopram over the antidepressants citalopram andfluoxetine in the first two weeks of major depression.[6] Concerns of sponsorship bias with the studies are however noted.[6] In another review escitalopram and sertraline had the highest rate of efficacy and acceptability among adults receiving treatment for major depression with second-generation antidepressants.[7]

Efficacy

There is some controversy over selective publishing of SSRI clinical trials.[8] A meta-analysis analyzing published as well as unpublished trials found placebos to be similarly effective to SSRIs in treating mild depression, although SSRIs were more effective than placebo in more severe cases, with the magnitude of SSRI superiority increasing with increasing depression severity.[9]

A series of randomized, double-blind trials have found Escitalopram to be more efficacious and have fewer adverse effects than Citalopram.[10][11][12][13] Meta-analysis show a “small” but statistically significant improvement in effect strength [14][15] and some dispute these findings.[16]

Pharmacology

Cipralex brand escitalopram 10mg package and tablet sheet

Escitalopram increases intrasynaptic levels of the neurotransmitter serotonin by blocking the reuptake of the neurotransmitter into the presynaptic neuron. Of the SSRIs currently on the market, escitalopram has the highest affinity for the human serotonin transporter (SERT). The enantiomer of escitalopram ((R)-citalopram) counteracts to a certain degree the serotonin-enhancing action of escitalopram. As a result, escitalopram has been claimed to be a more potent antidepressant than citalopram, which is a mixture of escitalopram and (R)-citalopram. In order to explain this phenomenon, researchers from Lundbeck proposed that escitalopram enhances its own binding via an additional interaction with another allosteric site on the transporter.[42] Further research by the same group showed that (R)-citalopram also enhances binding of escitalopram,[43] and therefore the allosteric interaction cannot explain the observed counteracting effect. In the most recent paper, however, the same authors again reversed their findings and reported that R-citalopram decreases binding of escitalopram to the transporter.[44] Although allosteric binding of escitalopram to the serotonin transporter is of unquestionable research interest, its clinical relevance is unclear since the binding of escitalopram to the allosteric site is at least 1000 times weaker than to the primary binding site.

In vitro studies using human liver microsomes indicated that CYP3A4 and CYP2C19 are the primary isozymes involved in the N-demethylation of escitalopram. The resulting metabolites, desmethylescitalopram and didesmethylescitalopram, are significantly less active and their contribution to the overall action of escitalopram is negligible.

History

Escitalopram was developed in close cooperation between Lundbeck and Forest Laboratories. Its development was initiated in the summer of 1997, and the resulting new drug application was submitted to the U.S. FDA in March 2001. The short time (3.5 years) it took to develop escitalopram can be attributed to the previous extensive experience of Lundbeck and Forest with citalopram, which has similar pharmacology.[45] The FDA issued the approval of escitalopram for major depression in August 2002 and for generalized anxiety disorder in December 2003. Escitalopram can be considered an example of “evergreening“[46] (also called “lifecycle management”[47])– the long-term strategy pharmaceutical companies use in order to extend the lifetime of a drug, in this case of the citalopram franchise. Escitalopram is an enantiopure compound of theracemic mixture citalopram, used for the same indication, and for that reason it required less investment and less time to develop. Two years after escitalopram’s launch, when the patent on citalopram expired, the escitalopram sales successfully made up for the loss. On May 23, 2006, the FDA approved a generic version of escitalopram by Teva.[48]On July 14 of that year, however, the U.S. District Court of Delaware decided in favor of Lundbeck regarding the patent infringement dispute and ruled the patent on escitalopram valid.[49]

In 2006 Forest Laboratories was granted an 828 day (2 years and 3 months) extension on its US patent for escitalopram.[50] This pushed the patent expiration date from December 7, 2009 to September 14, 2011. Together with the 6-month pediatric exclusivity, the final expiration date was March 14, 2012.

Brand names

Escitalopram is sold under the following brand names:

  • Animaxen (Colombia)
  • Anxiset-E (India)
  • Cipralex
  • Escital (Nigeria)
  • Citalin
  • Citram (Croatia)
  • Ecytara (Slovenia)
  • Elicea
  • Entact (Greece)
  • Escitalopram Actavis (Finland)
  • Escitil (Czech Republic)
  • Esitalo (Australia)
  • Esopram, by Actavis (Iceland)
  • Esto (Israel)
  • Escitalopram Teva (Israel)
  • Exodus (Brazil)
  • Lexam
  • Lexamil (South Africa)
  • Lexapro
  • Losita (Bangladesh)
  • Nexito
  • Reposil (Chile)
  • Selectra (Russia)
  • Selpram (Pakistan)
  • Seroplex
  • Sipralexa (Belgium)

References

  1. ^ a b c NHS pays millions of pounds more than it needs to for drugs, The Independent. Retrieved 05/10/2011.
  2. ^ “Escitalopram Oxalate”. The American Society of Health-System Pharmacists. Retrieved 3 April 2011.
  3. ^ Kasper, S; Stein, DJ; Loft, H; Nil, R (2005). “Escitalopram in the treatment of social anxiety disorder: Randomised, placebo-controlled, flexible-dosage study”. The British journal of psychiatry : the journal of mental science 186 (3): 222–6.doi:10.1192/bjp.186.3.222. PMID 15738503.
  4. ^ Stahl, SM; Gergel, I; Li, D (2003). “Escitalopram in the treatment of panic disorder: A randomized, double-blind, placebo-controlled trial”. The Journal of clinical psychiatry 64(11): 1322–7. PMID 14658946.
  5. ^ Stein, DJ; Andersen, EW; Tonnoir, B; Fineberg, N (2007). “Escitalopram in obsessive-compulsive disorder: A randomized, placebo-controlled, paroxetine-referenced, fixed-dose, 24-week study”. Current medical research and opinion 23 (4): 701–11. doi:10.1185/030079907X178838. PMID 17407626.
  6. ^ a b Cipriani, A; Santilli C; Furukawa TA; Signoretti A; Nakagawa A; McGuire H; Churchill R; Barbui C (2009 April 15). “Escitalopram versus other antidepressant agents for depression”. In Cipriani, Andrea. Cochrane database of systematic reviews(2): CD006532. doi:10.1002/14651858.CD006532.pub2. PMID 19370639. CD006532.
  7. ^ Cipriani, A; Furukawa TA; Salanti G; Geddes JR; Higgins JP; Churchill R; Watanabe N; Nakagawa A; Omori IM; McGuire H; Tansella M; Barbui C (2009 February 28). “Comparative efficacy and acceptability of 12 new-generation antidepressants: a multiple-treatments meta-analysis”. Lancet 373 (9665): 746–58. doi:10.1016/S0140-6736(09)60046-5. PMID 19185342.
  8. ^ Ioannidis JP (2008). “Effectiveness of antidepressants: an evidence myth constructed from a thousand randomized trials?”. Philos Ethics Humanit Med 3: 14.doi:10.1186/1747-5341-3-14. PMC 2412901. PMID 18505564.
  9. ^ Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J (January 2010). “Antidepressant drug effects and depression severity: a patient-level meta-analysis”. JAMA 303 (1): 47–53. doi:10.1001/jama.2009.1943.PMID 20051569.
  10. ^ Ou, JJ; Xun, GL; Wu, RR; Li, LH; Fang, MS; Zhang, HG; Xie, SP; Shi, JG; Du, B; Yuan, XQ; Zhao, JP (2011 Feb). “Efficacy and safety of escitalopram versus citalopram in major depressive disorder: a 6-week, multicenter, randomized, double-blind, flexible-dose study.”. Psychopharmacology 213 (2-3): 639–46. doi:10.1007/s00213-010-1822-y. PMID 20340011. |accessdate= requires |url= (help)
  11. ^ Yevtushenko, VY; Belous, AI; Yevtushenko, YG; Gusinin, SE; Buzik, OJ; Agibalova, TV (2007 Nov). “Efficacy and tolerability of escitalopram versus citalopram in major depressive disorder: a 6-week, multicenter, prospective, randomized, double-blind, active-controlled study in adult outpatients.”. Clinical therapeutics 29 (11): 2319–32.PMID 18158074.
  12. ^ Colonna, L; Andersen, HF; Reines, EH (2005 Oct). “A randomized, double-blind, 24-week study of escitalopram (10 mg/day) versus citalopram (20 mg/day) in primary care patients with major depressive disorder.”. Current medical research and opinion 21(10): 1659–68. PMID 16238906.
  13. ^ Moore, N; Verdoux, H; Fantino, B (2005 May). “Prospective, multicentre, randomized, double-blind study of the efficacy of escitalopram versus citalopram in outpatient treatment of major depressive disorder.”. International clinical psychopharmacology 20 (3): 131–7. PMID 15812262.
  14. ^ Montgomery, Stuart; Hansen, Thomas; Kasper, Siegfried (28 September 2010). “Efficacy of escitalopram compared to citalopram: a meta-analysis”. The International Journal of Neuropsychopharmacology 14 (02): 261–268.doi:10.1017/S146114571000115X. PMID 20875220.
  15. ^ Gorman, JM; Korotzer, A; Su, G (2002 Apr). “Efficacy comparison of escitalopram and citalopram in the treatment of major depressive disorder: pooled analysis of placebo-controlled trials.”. CNS spectrums 7 (4 Suppl 1): 40–4. PMID 15131492.
  16. ^ Trkulja, V (2010 Feb). “Is escitalopram really relevantly superior to citalopram in treatment of major depressive disorder? A meta-analysis of head-to-head randomized trials.”. Croatian medical journal 51 (1): 61–73. PMID 20162747.
  17. ^ “Citalopram and escitalopram: QT interval prolongation—new maximum daily dose restrictions (including in elderly patients), contraindications, and warnings”.Medicines and Healthcare products Regulatory Agency. December 2011. Retrieved March 5, 2013.
  18. ^ Van Gorp, Freek; Whyte, Ian M.; Isbister, Geoffrey K. (2009). “Clinical and ECG Effects of Escitalopram Overdose”. Annals of Emergency Medicine 54 (3): 404–8.doi:10.1016/j.annemergmed.2009.04.016. PMID 19556032.
  19. ^ FDA Center for Drug Evaluation and Research (2001). “Review and evaluation of clinical data for application 21-323”. Retrieved 2009-12-03.
  20. ^ Bolton JM, Sareen J, Reiss JP (2006). “Genital anesthesia persisting six years after sertraline discontinuation”. J Sex Marital Ther 32 (4): 327–30.doi:10.1080/00926230600666410. PMID 16709553.
  21. ^ Clayton A, Keller A, McGarvey EL (2006). “Burden of phase-specific sexual dysfunction with SSRIs”. Journal of Affective Disorders 91 (1): 27–32.doi:10.1016/j.jad.2005.12.007. PMID 16430968.
  22. ^ Lexapro prescribing information
  23. ^ Csoka AB, Bahrick AS, Mehtonen O-P (2008). “Persistent Sexual Dysfunction after Discontinuation of Selective Serotonin Reuptake Inhibitors (SSRIs)”. J Sex Med. 5 (1): 227–33. doi:10.1111/j.1743-6109.2007.00630.x. PMID 18173768.
  24. ^ Baldwin DS, Reines EH, Guiton C, Weiller E (2007). “Escitalopram therapy for major depression and anxiety disorders”. Ann Pharmacother 41 (10): 1583–92.doi:10.1345/aph.1K089. PMID 17848424.
  25. ^ Pigott TA, Prakash A, Arnold LM, Aaronson ST, Mallinckrodt CH, Wohlreich MM (2007). “Duloxetine versus escitalopram and placebo: an 8-month, double-blind trial in patients with major depressive disorder”. Curr Med Res Opin 23 (6): 1303–18.doi:10.1185/030079907X188107. PMID 17559729.
  26. ^ Davidson JR, Bose A, Wang Q (2005). “Safety and efficacy of escitalopram in the long-term treatment of generalized anxiety disorder”. J Clin Psychiatry 66 (11): 1441–6.doi:10.4088/JCP.v66n1115. PMID 16420082.
  27. ^ Kasper S, Lemming OM, de Swart H (2006). “Escitalopram in the long-term treatment of major depressive disorder in elderly patients”. Neuropsychobiology 54 (3): 152–9. doi:10.1159/000098650. PMID 17230032.
  28. ^ Guerdjikova, AI; McElroy SL, Kotwal R, et al. (January 2008). “High-dose escitalopram in the treatment of binge-eating disorder with obesity: a placebo-controlled monotherapy trial”. Human Psychopharmacology: Clinical and Experimental23 (1): 1–11. doi:10.1002/hup.899. PMID 18058852.
  29. ^ Levenson M, Holland C. “Antidepressants and Suicidality in Adults: Statistical Evaluation. (Presentation at Psychopharmacologic Drugs Advisory Committee; December 13, 2006)”. Retrieved 2007-05-13.
  30. ^ Stone MB, Jones ML (2006-11-17). “Clinical Review: Relationship Between Antidepressant Drugs and Suicidality in Adults” (PDF). Overview for December 13 Meeting of Pharmacological Drugs Advisory Committee (PDAC). FDA. pp. 11–74. Retrieved 2007-09-22.
  31. ^ Levenson M; Holland C (2006-11-17). “Statistical Evaluation of Suicidality in Adults Treated with Antidepressants” (PDF). Overview for December 13 Meeting of Pharmacological Drugs Advisory Committee (PDAC). FDA. pp. 75–140. Retrieved 2007-09-22.
  32. ^ Gunnell D, Saperia J, Ashby D (2005). “Selective serotonin reuptake inhibitors (SSRIs) and suicide in adults: meta-analysis of drug company data from placebo controlled, randomized controlled trials submitted to the MHRA’s safety review”. BMJ330 (7488): 385. doi:10.1136/bmj.330.7488.385. PMC 549105. PMID 15718537.
  33. ^ Khan A, Schwartz K (2007). “Suicide risk and symptom reduction in patients assigned to placebo in duloxetine and escitalopram clinical trials: analysis of the FDA summary basis of approval reports”. Ann Clin Psychiatry 19 (1): 31–6.doi:10.1080/10401230601163550. PMID 17453659.
  34. ^ Budur, Kumar; Hutzler, Jeffrey (June 2004). “Severe suicidal ideation with escitalopram (Lexapro): a case report”. Primary Care Psychiatry 9 (2): 67–68.doi:10.1185/135525704125004222.
  35. ^ Karch, Amy (2006). 2006 Lippincott’s Nursing Drug Guide. Philadelphia, Baltimore, New York, London, Buenos Aires, Hong Kong, Sydney, Tokyo: Lippincott Williams & Wilkins. ISBN 1-58255-436-6.
  36. ^ Malling, D.; Poulsen, M.; Søgaard, B. (2005). “The effect of cimetidine or omeprazole on the pharmacokinetics of escitalopram in healthy subjects”. British Journal of Clinical Pharmacology 60 (3): 287–290. doi:10.1111/j.1365-2125.2005.02423.x.PMC 1884771. PMID 16120067. edit
  37. ^ “Lexapro – Warnings”. RxList. 12/08/2004. Retrieved 2006-10-22.
  38. ^ Alwan S, Reefhuis J, Rasmussen SA, Olney RS, Friedman JM, for the National Birth Defects Prevention Study. Use of selective serotonin-reuptake inhibitors in pregnancy and the risk of birth defects. N Engl J Med 2007;356:2684–92.
  39. ^ van Gorp F, Whyte IM, Isbister GK. Clinical and ECG effects of escitalopram overdose. Ann. Emer. Med. 54: 404-408, 2009.
  40. ^ Haupt D. Determination of citalopram enantiomers in human plasma by liquid chromatographic separation on a Chiral-AGP column. J. Chrom. B 685: 299-305, 1996.
  41. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 552-553.
  42. ^ For an overview of supporting data, see Sánchez C, Bøgesø KP, Ebert B, Reines EH, Braestrup C (2004). “Escitalopram versus citalopram: the surprising role of the R-enantiomer”. Psychopharmacology (Berl.) 174 (2): 163–76. doi:10.1007/s00213-004-1865-z. PMID 15160261.
  43. ^ Chen F, Larsen MB, Sánchez C, Wiborg O (2005). “The (S)-enantiomer of (R,S)-citalopram, increases inhibitor binding to the human serotonin transporter by an allosteric mechanism. Comparison with other serotonin transporter inhibitors”.European Neuropsychopharmacology 15 (2): 193–198.doi:10.1016/j.euroneuro.2004.08.008. PMID 15695064.
  44. ^ Mansari ME, Wiborg O, Mnie-Filali O, Benturquia N, Sánchez C, Haddjeri N (2007). “Allosteric modulation of the effect of escitalopram, paroxetine and fluoxetine: in-vitro and in-vivo studies”. The International Journal of Neuropsychopharmacology 10 (1): 31–40. doi:10.1017/S1461145705006462. PMID 16448580.
  45. ^ “2000 Annual Report. p 28 and 33” (PDF). Lundbeck. 2000. Retrieved 2007-04-07.
  46. ^ “”New drugs from old”. Presented at the Medical Journal Club, Morriston Hospital, by Scott Pegler, pharmacist at the National Health Service, UK, on November 20, 2006.” (PPT). Retrieved 2007-04-07.
  47. ^ “New drugs from old”. Drug and Therapeutics Bulletin (BMJ Publishing Group Ltd.)44 (10): 73–77. 2006. doi:10.1136/dtb.2006.441073. PMID 17067118.
  48. ^ Miranda Hitti. “FDA OKs Generic Depression Drug – Generic Version of Lexapro Gets Green Light”. WebMD. Retrieved 2007-10-10.
  49. ^ Marie-Eve Laforte (2006-07-14). “US court upholds Lexapro patent”. FirstWord. Retrieved 2007-10-10.
  50. ^ “Forest Laboratories Receives Patent Term Extension for Lexapro” (Press release). PRNewswire-FirstCall. 2006-03-02. Retrieved 2009-01-19.
  51. ^ Harris, “A Drug Maker’s Playbook Reveals a Marketing Strategy”
  52. ^ Lexapro Fiscal 2004 Marketing Plan
  53. ^ “Forest Laboratories: A Tale of Two Whistleblowers” article by Alison Frankel inThe American Lawyer February 27, 2009
  54. ^ United States of America v. Forest Laboratories Full text of the federal complaint filed in the US District Court for the district of Massachusetts
  55. ^ “Drug Maker Is Accused of Fraud” article by Barry Meier and Benedict Carey inThe New York Times February 25, 2009
  56. ^ “Forest Laboratories, Inc. Provides Statement in Response to Complaint Filed by U.S. Government” Forest press-release. February 26, 2009.

 

 

 

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http://www.sciencedirect.com/science/article/pii/S0040402011015249

 

http://www.sciencedirect.com/science/article/pii/S0040402011015249

 

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AstraZeneca pays $50 million upfront for Merck & Co cancer drug

 Uncategorized  Comments Off on AstraZeneca pays $50 million upfront for Merck & Co cancer drug
Sep 122013
 

AstraZeneca has licensed a drug which is in mid-stage studies for ovarian cancer from Merck & Co.

The pact centres around the US drug major’s MK-1775, an oral small molecule inhibitor of WEE1 kinase, a cell cycle checkpoint protein regulator. Preclinical data indicate that disruption of WEE1 may enhance the cell killing effects of some anticancer agents and the compound is in Phase IIa studies in combination with standard of care therapies for the treatment of patients with certain types of ovarian cancer………….read all at

http://www.pharmatimes.com/Article/13-09-11/AZ_pays_50_million_upfront_for_Merck_Co_cancer_drug.aspx

MK-1775

MK-1775 is a potent and selective Wee1 inhibitor with IC50 of 5.2 nM; hinders G2 DNA damage checkpoint. Phase 2. IC50 of 5.2 nM

Chemical Name: 1,2-dihydro-1-[6-(1-hydroxy-1-methylethyl)-2-pyridinyl]-6-[[4-(4-methyl-1-piperazinyl)phenyl]amino]-2-(2-propen-1-yl)-3H-Pyrazolo[3,4-d]pyrimidin-3-one

Elemental Analysis: C, 64.78; H, 6.44; N, 22.38; O, 6.39

CAS 955365-80-7

C27H32N8O2

MW 500.61

Biological Activity:

 

A potent and selective Wee1 kinase inhibitor in vitro and in vivo.

 

MK 1775 abolishes cyclin-dependent kinase 1 (CDC2) activity by phosphorylation of the Tyr15 residue. It abrogates a DNA damage checkpoint (G2-phase), leading to apoptosis in combination with several DNA-damaging agents selectively in p53-deficient tumor cell lines. It is under clinical trial for advanced solid tumors.

 

References:  

 

H. Hirai et al. Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents. Mol. Cancer. Ther. 2009, 8(11), 2992-3000. [online]

 

S. Schellens et al. A Phase I and pharmacological study of MK-1775, a Wee1 tyrosine kinase inhibitor, in both monotherapy and in combination with gemcitabine, cisplatin, or carboplatin in patients with advanced solid tumors. J. Clin. Oncol. 2009, 27(15s), abstr 3510.

 

H. Hirai et al. MK-1775, a small molecule Wee1 inhibitor, enhances anti-tumor efficacy of various DNA-damaging agents, including 5-fluorouracil. Cancer Biol. Ther. 2010, 9(7), 523-525. [online]

 

CC Porter et al. Integrated genomic analyses identify WEE1 as a critical mediator of cell fate and a novel therapeutic target in acute myeloid leukemia. Leukemia 2012, 26, 1266-1276.  [online]

 

MK-1775 is an inhibitor of Wee1, a kinase that phosphorylates CDC2 to inactivate the CDC2/cyclin B complex (regulating the G2 checkpoint). Since most human cancers harbor p53-dependent G1 checkpoint abnormalities, they are dependent on the G2 checkpoint. G2 checkpoint abrogation may therefore sensitize p53 deficient tumor cells to anti-cancer agents

 

MK-1775 inhibits phosphorylation of CDC2 at Tyr15 (CDC2Y15), a direct substrate of Wee1 kinase in cells. MK-1775 abrogates G2 DNA damage checkpoint, leading to apoptosis in combination with DNA-damaging chemotherapeutic agents such as gemcitabine, carboplatin, and cisplatin selectively in p53-deficient cells. In vivo, MK-1775 potentiates tumor growth inhibition by these agents, and cotreatment does not significantly increase toxicity. The enhancement of antitumor effect by MK-1775 was well correlated with inhibition of CDC2Y15 phosphorylation in tumor tissue and skin hair follicles. Our data indicate that Wee1 inhibition provides a new approach for treatment of multiple human malignancies. [Mol Cancer Ther 2009;8(11):2992-3000].

 

MK-1775 is a first in class Wee1 inhibitor that is well tolerated and shows promising anti-tumor activity in previously treated pts. for detail see: http://meeting.ascopubs.org/cgi/content/abstract/27/15S/3510.

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Drug in Focus: Abiraterone Acetate (Zytiga) New drug for the treatment of advanced prostate cancer

 cancer  Comments Off on Drug in Focus: Abiraterone Acetate (Zytiga) New drug for the treatment of advanced prostate cancer
Sep 112013
 

Abiraterone Acetate (Zytiga)

When prostate cancer spreads to another location in the body, it is considered to have metastasised, and surgery to remove the prostate and pelvic lymph nodes cannot eliminate the cancer. As a result, most men with metastatic prostate cancer (PCa) receive hormonal therapy which is also known as androgen ablation or androgen-deprivation therapy (ADT). ADT is used to reduce the levels of circulating androgens (male hormones) in the body (a process known as castration) or to keep them from reaching PCa cells. After sometime, however, the PCa no longer responds to hormone therapy, including LHRH analogues and anti-androgens, andis considered to be castration-resistant. At this stage, so-called metastatic castration-resistant PCa (mCRPC) becomes increasingly difficult to treat……………full article

 

READ ALL AT

http://www.medicalgrapevineasia.com/mg/2013/07/09/drug-in-focus-abiraterone-acetate-zytiga/

by

Dr Tan Yew Oo, Medical Oncologist and Hematologist in private practice at Gleneagles Hospital, to tell us more about AA.

Dr Tan Yew Oo is currently a Consultant Medical Oncologist and Hematologist in private practice at Gleneagles Hospital, Singapore. After graduating with MBBS from University of Singapore in 1971, he did his postgraduate training in Internal Medicine, Hematology and Medical Oncology in the United States and Canada. Upon his return to Singapore, he joined the Faculty of Medicine of the National University of Singapore in 1978 as Lecturer. He rapidly rose to be Chief of Medicine at National University Hospital (NUH) and Head, Division of Hematology-Oncology at NUH in 1988 and Professor of Medicine in 1991. He resigned and went into private practice since 1993. Dr Tan has been active in post-graduate education and has published many papers and has been an invited speaker for numerous meetings. He has participated in several international phase III clinical trials using novel drugs, and he has special interests in multiple myeloma, breast, thoracic and GI/GU oncology.

 

 

Chemical synthesis of Abiraterone acetate

The following synthetic route of Abiraterone acetate was  from J Med Chem. 1995 Jun 23;38(13):2463-71. Novel steroidal inhibitors of human cytochrome P45017 alpha (17 alpha-hydroxylase-C17,20-lyase): potential agents for the treatment of prostatic cancer. Potter GA, Barrie SE, Jarman M, Rowlands MG. Cancer Research Campaign Centre for Cancer Therapeutics, Institute of Cancer Research, Sutton, Surrey, U.K.

 

CAS#: 154229-18-2.

Synonym: CB 7630；CB-7630.

Chemical Formula: C26H33NO2
Exact Mass: 391.25113
Molecular Weight: 391.54
Elemental Analysis: C, 79.76; H, 8.50; N, 3.58; O, 8.17

IUPAC: [(3S,10R,13S)-10,13-dimethyl-17-pyridin-3-yl-2,3,4,7,8,9,11,12,14,15-decahydro-1H-cyclopenta[a]phenanthren-3-yl] acetate.

 

 

 

ZYTIGA™ (abiraterone acetate) received FDA Approval  in May 2011 for Treatment of Metastatic Prostate Cancer After Priority Review; First Once-Daily, Oral Treatment for Metastatic Prostate Cancer Inhibits Androgen Production. ZYTIGA™ (abiraterone acetate) in combination with prednisone is indicated for the treatment of patients with metastatic castration-resistant prostate cancer (CRPC) who have received prior chemotherapy containing docetaxel.

 

According to Wikipedia, Abiraterone (tradename Zytiga) is a drug currently under investigation for use in castration-resistant prostate cancer (formerly hormone-resistant or hormone-refractory prostate cancer) (prostate cancer not responding to androgen deprivation or treatment with antiandrogens). After an expedited six-month review, the drug has been approved for use by the Food and Drug Administration (FDA). This drug was initially discovered in the Cancer Research UK Centre for Cancer Therapeutics at the Institute of Cancer Research in London. Rights for commercialization of the drug were assigned to BTG plc, a UK company that manages commercialization activity in pharmaceuticals. BTG then licensed the product to Cougar Biotechnology which began development of the commercial product.  In 2009, Cougar was acquired by Johnson & Johnson which is currently conducting clinical trials on abiraterone.   http://en.wikipedia.org/wiki/Abiraterone). 

Abiraterone acetate is an FDA approved drug, and is an orally active acetate ester of the steroidal compound abiraterone with antiandrogen activity. Abiraterone acetate was approved by the U.S. Food and Drug Administration (FDA) in April 2011. Abiraterone inhibits the enzymatic activity of steroid 17alpha-monooxygenase (17alpha-hydrolase/C17,20 lyase complex), a member of the cytochrome p450 family that catalyzes the 17alpha-hydroxylation of steroid intermediates involved in testosterone synthesis. Administration of this agent may suppress testosterone production by both the testes and the adrenals to castrate-range levels. Check for active clinical trials or closed clinical trials using this agent.

 

Current developer:  Cougar Biotechnology Inc, and Johnson & Johnson。

 

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Comparing China’s And India’s Pharmaceutical Manufacturing

 china, INDIA  Comments Off on Comparing China’s And India’s Pharmaceutical Manufacturing
Sep 112013
 

By Jim Zhang, Ph.D., JZMed, Inc.

The pharmaceutical markets of China and India have been experiencing such rapid growth in the past decade that they are widely recognized as two of the world’s most dynamic emerging markets. Consequently, they have attracted many drug companies around the world…………FULL ARTICLE

READ ALL AT

http://www.pharmaceuticalonline.com/doc/comparing-china-s-and-india-s-pharmaceutical-manufacturing-0001

Jim Zhang, Ph.D., is president and managing director of JZMed, Inc., a market research company specializing in research on the Chinese pharmaceutical outsourcing industry. The company also provides consulting services for pharmaceutical outsourcing in China.

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Melatonin: It’s Not Just for Bedtime Anymore – Part 1

 Uncategorized  Comments Off on Melatonin: It’s Not Just for Bedtime Anymore – Part 1
Sep 102013
 

melatonin 300x200

Melatonin is a neurohormone that is produced in the brain, primarily by the pineal gland, from the amino acid tryptophan. Its most well known functions include helping to regulate sleep and the body’s circadian rhythm.

The amount of melatonin we produce is determined by how dark or light our surroundings are. Our eyes have specialized light-sensitive receptors that relay this message to a cluster of nerves in the brain called the suprachiasmatic nucleus, or SCN. The SCN sets our internal biological clock (circadian rhythm) while also regulating sleep. When our surroundings are dark, the SCN tells the pineal gland to produce melatonin, which is thought to trigger sleep. Some melatonin is also made in the stomach and intestines.

Melatonin: It’s Not Just for Bedtime Anymore – Part 1 read all at

http://blog.designsforhealth.com/blog/bid/186477/Melatonin-It-s-Not-Just-for-Bedtime-Anymore-Part-1#!

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Mallinckrodt PLC : Mallinckrodt Pharmaceuticals Announces Positive Phase 3 Efficacy Results for MNK-795, an Extended-Release Oxycodone/Acetaminophen Combination

 Phase 3 drug  Comments Off on Mallinckrodt PLC : Mallinckrodt Pharmaceuticals Announces Positive Phase 3 Efficacy Results for MNK-795, an Extended-Release Oxycodone/Acetaminophen Combination
Sep 062013
 

MALLINCKRODT PLC : Mallinckrodt Pharmaceuticals Announces Positive …
4-traders (press release)
Mallinckrodt (NYSE: MNK) today reported data that investigational drug MNK-795 achieved the primary endpoint in a Phase 3 efficacy trial in the treatment of acute pain following a bunionectomy.

In the study, MNK-795 showed statistically significant …http://www.4-traders.com/MALLINCKRODT-PLC-13450292/news/Mallinckrodt-PLC–Mallinckrodt-Pharmaceuticals-Announces-Positive-Phase-3-Efficacy-Results-for-MNK-17242621/

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This Biotech Has So Many Reasons to Be Liked

 Uncategorized  Comments Off on This Biotech Has So Many Reasons to Be Liked
Sep 062013
 

This Biotech Has So Many Reasons to Be Liked
Motley Fool
With promising mid-stage results, the drug is expected to do well in phase 3 evaluation for pancreatic cancer.

Positive phase 3 results will open the door to the lucrative pancreatic cancer market, on top of the myelofibrosis market that is expected to …

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http://www.fool.com/investing/general/2013/09/05/this-biotech-has-so-many-reasons-to-be-liked.aspx

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Oramed Submits Pre-IND Package to FDA for ORMD-0901 (oral exenatide)

 Uncategorized  Comments Off on Oramed Submits Pre-IND Package to FDA for ORMD-0901 (oral exenatide)
Sep 042013
 

Oramed Submits Pre-IND Package to FDA for ORMD-0901 (oral exenatide), an …
MarketWatch
JERUSALEM, September 3, 2013 /PRNewswire via COMTEX/ — Oramed Pharmaceuticals Inc. (nasdaqcm:ORMP) (http://www.oramed.com), a developer of oral drug delivery systems, announced today that it has submitted a pre-Investigational New Drug … capsule …

http://www.marketwatch.com/story/oramed-submits-pre-ind-package-to-fda-for-ormd-0901-oral-exenatide-an-oral-glp-1-analog-for-the-treatment-of-type-2-diabetes-2013-09-03?reflink=MW_news_stmp

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