Erica Thiel Age 31 WI I work for a rare disease foundation doing advocacy work w/MPS related to research and family outreach. I Live with MPS I Hurler Scheie /Scheie Syndrome a type of mucopolysaccharidoses, (lysosomal)disorder. I have been receiving enzyme replacement infusions since May 05. I have had approx 60+ surgeries and procedures in just the last 6 years including 30+ shunt revisions for commun. hydrocephalus in 3 years and and now have an programmable TPL an VP shunts to control pressure. C-spine decompression/fusion, lumbar laminectomies, Port placement, thenar tendon transfer, etc. For past blog entries see: www.caringbridge.org/wi/ericathiel I Love being an aunt - the very best feeling in the world! Being an aunt is particularly rewarding since I personally wont ever be a Mom to my own kids (by choice). MPS 1 Empowers study
FDA clearance to initiate Phase 1/2 clinical trials for SB-318 (MPS I) therapeutic program. Sangamo submitted the additional in vitro studies requested by the FDA in September 2016 and recently received clearance to initiate Phase 1/2 clinical trials for the Mucopolysaccharidosis Type I (MPS I, Hurler syndrome) based on its ZFN-mediated in vivo genome editing therapeutic platform. The company expects to initiate the clinical studies in early 2017.
Estimated Enrollment: 9 Actual Study Start Date: May 24, 2017 Estimated Study Completion Date: January 2022
The objectives of the study are to provide long term expression of IDUA and improve the current clinical outcome of enzyme replacement therapy (ERT) or hematopoietic stem cell transplantation (HSCT) therapy in subjects with attenuated MPS I, a recessive lysosomal storage disorder that results from mutations in the gene encoding IDUA. SB-318 is a therapeutic for ZFN-mediated genome editing which will be delivered by adeno-associated virus (AAV)-derived vectors. SB-318 is intended to function by placement of the corrective copy of the IDUA transgene into the genome of the subject's own hepatocytes, under the control of the highly expressed endogenous albumin locus, and is expected to provide permanent, liver-specific expression of iduronidase for the lifetime of an MPS I patient.
December 07, 2017 RICHMOND, Calif., Dec. 7, 2017 /PRNewswire/ -- Sangamo Therapeutics, Inc. (NASDAQ: SGMO) announced today that the Committee for Orphan Medicinal Products of the European Medicines Agency (EMA) has issued a positive opinion on the application for orphan medicinal product designation (OMPD) for SB-318 and SB-913, Sangamo's genome editing product candidates for the treatment of rare lysosomal storage disorders Mucopolysaccharidosis Type I (MPS I) and MPS II, respectively.
Sangamo Therapeutics, Inc. (PRNewsFoto/Sangamo BioSciences, Inc.) (PRNewsFoto/)
The EMA's OMPD is granted to medicines intended for the treatment, prevention or diagnosis of life-threatening or chronically debilitating conditions that are rare and affect less than five in 10,000 persons in the European Union (EU). The designation provides incentives to advance the development and commercialization of orphan medicines, which include access to the EU centralized authorization procedure and potential for market exclusivity for a period of up to ten years.
MPS I and MPS II are caused by mutations in the genes encoding alpha-L-iduronidase (IDUA) and iduronate 2-sulfatase (IDS) enzymes, respectively. Using Sangamo's zinc finger nuclease (ZFN) genome editing technology, SB-318 (for MPS I) and SB-913 (for MPS II) are designed as a single treatment strategy intended to provide stable, continuous production of the IDUA or IDS enzyme for the lifetime of the patient.
SB-318 and SB-913 have already received Orphan Drug, Fast Track and Rare Pediatric Disease designations from the U.S. Food and Drug Administration (FDA). The Phase 1/2 clinical trials for these programs, evaluating SB-318 and SB-913 in adults with MPS I and MPS II, respectively, are open and enrolling subjects.
Sangamo's In Vivo Genome Editing Approach Sangamo's ZFN-mediated in vivo genome editing approach makes use of the endogenous albumin gene locus, a highly expressing and liver-specific site that can be edited with ZFNs to accept and express therapeutic genes. The approach is designed to enable the patient's liver to permanently produce circulating therapeutic levels of a corrective protein. The ability to permanently integrate the therapeutic gene in a highly specific, targeted fashion significantly differentiates Sangamo's in vivo genome editing approach from conventional AAV cDNA gene therapy. The design of these programs is ultimately to target a population that includes pediatric patients, and it will be important in this population to be able to produce stable levels of therapeutic protein for the lifetime of the patient.
Still no update for trial since Sept 26: Study Type : Interventional (Clinical Trial) Estimated Enrollment : 9 participants Allocation: Non-Randomized Intervention Model: Single Group Assignment Masking: None (Open Label) Primary Purpose: Treatment
Official Title: A Phase I, Multicenter, Open-label, Single-dose, Dose-ranging Study to Assess the Safety and Tolerability of SB-318, a rAAV2/6-based Gene Transfer in Subjects With Mucopolysaccharidosis I (MPS I)
Actual Study Start Date : May 24, 2017 Estimated Primary Completion Date : January 2020 Estimated Study Completion Date : January 2022
Regenxbio RGX-111 in Phase I/II RGX-111 is our product candidate for the treatment of Mucopolysaccharidosis Type I (MPS I), which is designed to use the AAV9 vector to deliver the human α-l-iduronidase (IDUA) gene to the central nervous system (CNS). MPS I is a rare recessive genetic disease caused by deficiency of IDUA, an enzyme required for the breakdown of polysaccharides heparan sulfate and dermatan sulfate in the lysosomes of cells. Many patients develop symptoms related to glycosaminoglycan storage in the CNS, which can include excessive accumulation of fluid in the brain (hydrocephalus), spinal cord compression and cognitive impairment.
Current standard of care treatments cannot treat the CNS manifestations of MPS I and leave a significant unmet need for a method to safely achieve long-term IDUA reconstitution in the CNS.
Delivery of the enzyme that is deficient within cells in the CNS could provide a permanent source of secreted IDUA beyond the blood-brain barrier, allowing for long-term cross correction of cells throughout the CNS.
The IND for RGX-111 for the treatment of MPS I is active and we expect to begin enrollment in a Phase I clinical trial in mid-2018. RGX-111 has received orphan drug product and rare pediatric disease designation from the FDA.
REGENXBIO’s gene therapy product candidates deliver genes to cells using adeno-associated virus (AAV) vectors, which are nonreplicating viral delivery vehicles that are not known to cause disease. Our product candidates all utilize viral vectors from our proprietary gene delivery platform, which we call our NAV Technology Platform.
Our NAV Technology Platform consists of exclusive rights to AAV7, AAV8, AAV9, AAVrh10 and over 100 other novel AAV vectors (NAV Vectors). We currently have exclusive rights to over 100 patents and patent applications worldwide covering our NAV Vectors, including composition of matter claims for AAV7, AAV8, AAV9 and AAVrh10, as well as methods for their manufacture and therapeutic uses. We believe this patent portfolio forms a strong foundation for our current programs and with our ongoing research and development, we expect to continue to expand this robust patent portfolio.
The foundation of our NAV Technology Platform was discovered in an effort to identify next generation AAV vectors that could overcome the limitations of earlier generation AAV vectors (AAV1 through AAV6). We believe the key benefits of NAV Vectors over earlier generation AAV vectors potentially include • Higher gene expression • Longer-term gene expression • Broad and novel tissue selectivity • Lower immune response • Improved manufacturability
We believe our NAV Technology Platform is proving to be a significant advancement over earlier AAV vectors in delivering these therapies. Based on data derived from third-party clinical studies and animal models using our NAV Vectors, we believe our NAV Technology Platform possesses unique, beneficial properties that are not seen in earlier generation AAVs. We believe that our NAV Technology Platform, which underpins our internal development programs and the programs of our NAV Technology Licensees, will enable us and our partners to develop best-in-class gene therapy candidates for a wide range of disease targets due to these unique properties.
Mucopolysaccharidosis type I (MPS I) is a condition that affects many parts of the body. This disorder was once divided into three separate syndromes: Hurler syndrome (MPS I-H), Hurler-Scheie syndrome (MPS I-H/S), and Scheie syndrome (MPS I-S), listed from most to least severe. Because there is so much overlap between each of these three syndromes, MPS I is currently divided into the severe and attenuated types.
Children with MPS I often have no signs or symptoms of the condition at birth, although some have a soft out-pouching around the belly-button (umbilical hernia) or lower abdomen (inguinal hernia). People with severe MPS I generally begin to show other signs and symptoms of the disorder within the first year of life, while those with the attenuated form have milder features that develop later in childhood.
Individuals with MPS I may have a large head (macrocephaly), a buildup of fluid in the brain (hydrocephalus), heart valve abnormalities, distinctive-looking facial features that are described as "coarse," an enlarged liver and spleen (hepatosplenomegaly), and a large tongue (macroglossia). Vocal cords can also enlarge, resulting in a deep, hoarse voice. The airway may become narrow in some people with MPS I, causing frequent upper respiratory infections and short pauses in breathing during sleep (sleep apnea).
People with MPS I often develop clouding of the clear covering of the eye (cornea), which can cause significant vision loss. Affected individuals may also have hearing loss and recurrent ear infections.
Some individuals with MPS I have short stature and joint deformities (contractures) that affect mobility. Most people with the severe form of the disorder also have dysostosis multiplex, which refers to multiple skeletal abnormalities seen on x-ray. Carpal tunnel syndrome develops in many children with this disorder and is characterized by numbness, tingling, and weakness in the hand and fingers. Narrowing of the spinal canal (spinal stenosis) in the neck can compress and damage the spinal cord.
While both forms of MPS I can affect many different organs and tissues, people with severe MPS I experience a decline in intellectual function and a more rapid disease progression. Developmental delay is usually present by age 1, and severely affected individuals eventually lose basic functional skills (developmentally regress). Children with this form of the disorder usually have a shortened lifespan, sometimes living only into late childhood. Individuals with attenuated MPS I typically live into adulthood and may or may not have a shortened lifespan. Some people with the attenuated type have learning disabilities, while others have no intellectual impairments. Heart disease and airway obstruction are major causes of death in people with both types of MPS I.
Mutations in the IDUA gene cause MPS I. The IDUA gene provides instructions for producing an enzyme that is involved in the breakdown of large sugar molecules called glycosaminoglycans (GAGs). GAGs were originally called mucopolysaccharides, which is where this condition gets its name. Mutations in the IDUA gene reduce or completely eliminate the function of the IDUA enzyme. The lack of IDUA enzyme activity leads to the accumulation of GAGs within cells, specifically inside the lysosomes. Lysosomes are compartments in the cell that digest and recycle different types of molecules. Conditions that cause molecules to build up inside the lysosomes, including MPS I, are called lysosomal storage disorders. The accumulation of GAGs increases the size of the lysosomes, which is why many tissues and organs are enlarged in this disorder. Researchers believe that the GAGs may also interfere with the functions of other proteins inside the lysosomes and disrupt the movement of molecules inside the cell.
CRISPR therapeutics has a "correction" editing approach in the research phase for MPS type I. This would appear to be at least 2 yrs from being in the clinic so I'll not be doing any research on them initially for the model.
MPS type I Hurler, Hurler-Scheie, Scheie syndrome MPS I is a mucopolysaccharide disease also called Hurler, Hurler-Scheie and Scheie syndrome. Hurler takes its name from Gertrude Hurler, the doctor who described a boy and girl with the condition in 1919. In 1962, Dr. Scheie, a consultant ophthalmologist, wrote about patients who were more mildly affected. Individuals who do not fit the severe or mild ends of the disease were said to have Hurler/Scheie. The specific disease names have been replaced with the designations attenuated (diminished severity) and severe MPS I. MPS I has a wide range of symptoms that vary in severity and can be managed and treated with enzyme replacement therapies. There is no cure for MPS I.
What causes this disease? Mucopolysaccharides are chains of sugar molecules used to build connective tissues in the body.
“muco” refers to the thick jelly-like consistency of the molecules “poly” means many “saccharide” is a general term for a sugar molecule The body constantly replaces used materials and breaks them down for disposal. MPS I patients are missing the enzyme alpha-L-iduronidase, which is essential in breaking down the mucopolysaccharides dermatan sulfate and heparan sulfate. These materials remain stored in the body’s cells, causing progressive damage. Babies may show little sign of the disease, but as cells sustain damage, symptoms start to appear.
Which disease does my child have? MPS I (Hurler-Scheie) is a continuum of severity based upon the symptoms, ranging from severe to attenuated. There is a great deal of variability of symptoms among individuals with MPS I, often making the specific designation difficult. Generally, severe MPS I will present within the first year of life while less severe (attenuated) forms present during childhood. Although individuals with attenuated MPS I have normal intelligence, they may have a variety of symptoms that can range from mild to severe.
How common are these diseases? Severe MPS I occurs in approximately 1 in 100,000 newborns. Attenuated MPS I is less common and occurs in about 1 in 500,000 newborns.
How is the disease inherited? MPS I (Hurler-Scheie syndrome ) is caused by a recessive gene. There is a one in four chance with every pregnancy that the child will inherit the defective gene from each carrier parent and will be affected with the disease. There is a two in three chance that unaffected brothers and sisters of children with MPS I will be carriers.
Is there cure for MPS I? There is no cure but treatments such as bone marrow transplantation and/or enzyme replacement therapy (ERT) can help make MPS I a more manageable disease. Aldurazyme is the first and only FDA approved ERT treatment developed through recombinant DNA technology for individuals with MPS I. For more information, visit the treatment website at www.aldurazyme.com.
Epidemiology Natl MPS society estimates 2,000 patients in the US (1 in 25,000) births - Severe MPS I 1 in 100k births - Attenuated MPS I 1 in 500k births mpssociety.org/learn/diseases/mps-i/
Epidemiology Prevalence is estimated at 1/100,000, with Hurler syndrome accounting for 57% of cases, Hurler-Scheie syndrome accounting for 23% of cases and Scheie syndrome accounting for 20% of cases.
Clinical description In the severe form (Hurler syndrome or MPS I-H; see this term) skeletal deformities and a delay in motor and intellectual development are the leading symptoms. Onset occurs 6-8 months after birth. Other manifestations include corneal clouding, organomegaly, heart disease, short stature, hernias, facial dysmorphism and hirsutism. Radiological examination of the skeleton reveals the characteristic pattern of dysostosis multiplex. Hydrocephaly can occur after the age of two. Patients with the adult-onset form (Scheie syndrome or MPS I-S; see this term) are of almost normal height and do not show intellectual deficiency. Typical symptoms are stiff joints, corneal opacities, carpal tunnel syndrome and mild skeletal changes. Aortic valve disease can be present. Compression of the cervical spinal cord, caused by glycosaminoglycan infiltration of the dura, may lead to spastic paresis if not corrected by neurosurgical intervention. Patients with the intermediate form (Hurler-Scheie syndrome or MPS I-H/S; see this term) have normal or almost normal intelligence, but exhibit various degrees of physical impairment.
Etiology The different phenotypes are caused by allelic mutations in the alpha-L-iduronidase (IDUA) gene (localized to 4p16.3). The mutations result in complete deficiency of the enzyme in Hurler syndrome or partial function in Scheie syndrome, leading to lysosomal accumulation of dermatan sulfate (DS) and heparan sulfate (HS). www.orpha.net/consor/cgi-bin/OC_Exp.php?Expert=579
MPS Subdivisions: Hurler syndrome (mucopolysaccharidosis type 1-H; MPS 1-H) is the most severe form of mucopolysaccharidosis. It is characterized by a deficiency of the enzyme alpha-L-iduronidase, which results in an accumulation of dermatan and heparan sulfates. Symptoms of the disorder first become evident at six months to two years of age. Affected infants may experience developmental delays, recurrent urinary and upper respiratory tract infections, noisy breathing and persistent nasal discharge. Additional physical problems may include clouding of the cornea of the eye, an unusually large tongue, severe deformity of the spine, and joint stiffness. Mental development begins to regress at about the age of two.
Scheie syndrome (mucopolysaccharidosis type I-S; MPS 1-S) is the mildest form of mucopolysaccharidosis. As in Hurler syndrome, individuals with Scheie syndrome have a deficiency of the enzyme alpha-L-iduronidase. However, in Scheie syndrome the deficiency is specific for accumulation of dermatan sulfate. Individuals with Scheie syndrome have normal intelligence, height, and life expectancy. Symptoms include stiff joints, carpal tunnel syndrome, backward flow of blood into the heart (aortic regurgitation), and clouding of the cornea that may result in the loss of visual acuity. The onset of symptoms in individuals with Scheie syndrome usually occurs around the age of five.
Hurler-Scheie syndrome (mucopolysaccharidosis type I-H/S; MPS-IH/S) is an extremely rare disorder that refers to individuals who have a less severe form of Hurler syndrome, but a more severe form than Scheie syndrome. Like Scheie syndrome, affected individuals have a deficiency of the alpha-L-iduronidase specific for accumulation of dermatan sulfate. Hurler-Scheie syndrome is not as severe as Hurler syndrome, but more severe than Scheie syndrome. Affected individuals may develop coarse facial features, joint stiffness, short stature, clouding of the corneas, abnormally enlarged liver and/spleen (hepatosplenomegaly), and skeletal and cardiac abnormalities. Intelligence may be normal or mild to moderate intellectual disability may develop. Symptoms usually become apparent between three and six years of age.
Hunter syndrome (mucopolysaccharidosis type II; MPS II) is the only type of MPS disorder inherited as an X-linked trait. Initial symptoms and findings associated with Hunter syndrome usually become apparent between ages two to four years. Such abnormalities may include progressive growth delays, resulting in short stature; joint stiffness, with associated restriction of movements; and coarsening of facial features, including thickening of the lips, tongue, and nostrils. Affected children may also have an abnormally large head (macrocephaly), a short neck and broad chest, delayed tooth eruption, progressive hearing loss, and enlargement of the liver and spleen (hepatosplenomegaly). Accumulation of heparin sulfate may occur. Two relatively distinct clinical forms of Hunter syndrome have been recognized. In the mild form of the disease (MPS IIB), intelligence may be normal or only slightly impaired. However, in the more severe form (MPS IIA), profound intellectual disability may become apparent by late childhood. In addition, slower disease progression tends to occur in those with the mild form of the disorder.
Sanfilippo syndrome (mucopolysaccharidosis type III; MPS III) has four subtypes (A, B, C, and D) that are distinguished by four different enzyme deficiencies. Initial symptoms of the four types of Sanfilippo syndrome include hyperactivity, sleep disorders, and delays in attaining developmental milestones (e.g., crawling and walking). All forms of Sanfilippo syndrome are characterized by varying degrees of intellectual disability, progressive loss of previously acquired skills (e.g., language), and hearing loss. Affected individuals may experience seizures, unsteady gait, and aggressive behavior. Affected individuals may eventually lose the ability to walk. Accumulation of heparan sulfate may occur.
Morquio syndrome (mucopolysaccharidosis type IV; MPS IV) exists in two forms (Morquio syndromes A and B) and occurs because of a deficiency of the enzyme N-acetyl-galactosamine-6-sulfatase and beta-galactosidase, respectively, resulting in accumulation of keratan and chondroitin sulfate in type A and keratan sulfate in type B. A deficiency of either enzyme leads to the accumulation of mucopolysaccharides in the body, abnormal skeletal development, and additional symptoms. In most cases, individuals with Morquio syndrome have normal intelligence. The clinical features of MPS IV-B are usually fewer and milder than those associated with MPS IV-A. Symptoms may include growth retardation, a prominent lower face, an abnormally short neck, knees that are abnormally close together (knock knees or genu valgum), flat feet, abnormal sideways and front-to-back or side-to-side curvature of the spine (kyphoscoliosis), abnormal development of the growing ends of the long bones (epiphyses), and/or a prominent breast bone (pectus carinatum). In some cases, hearing loss, weakness of the legs, and/or additional abnormalities also occurs.
Mucopolysaccharidosis type V is the former designation for Scheie syndrome. However when it was discovered that both Hurler and Scheie syndromes occur due to a deficiency of the same enzyme, Scheie syndrome was reclassified as a subtype of mucopolysaccharidosis type I.
Maroteaux-Lamy syndrome (mucopolysaccharidosis type VI; MPS VI) is characterized by a deficiency of the enzyme N-acetylgalactosamine-4-sulfatase, resulting in accumulation of dermatan sulfate. This form of MPS varies greatly among affected individuals. Some affected individuals only experience a few mild symptoms, other develop a more severe form of the disorder. Possible symptoms of Maroteaux-Lamy syndrome include coarse facial features, umbilical hernia, a prominent breast bone (pectus carinatum), joint contractures, clouding of the corneas, and an abnormal enlargement of the liver and/or spleen (heptasplenomegaly). Skeletal malformations and heart disease may occur in individuals with this form of MPS. In most cases, intelligence is normal.
Sly syndrome (mucopolysaccharidosis type VII; MPS VII) is characterized by a deficiency of the enzyme beta-glucuronidase, resulting in the accumulation of three glycosaminoglycans: dermatan sulfate, heparan sulfate and chondroitin sulfate. The symptoms may vary greatly from person to person. Individuals may have normal intelligence or mild to severe intellectual disability. Some skeletal abnormalities are often present. Hernias, clouding of the corneas, excessive accumulation of cerebrospinal fluid in the skull (hydrocephalus), short stature, heart disease, and coarse facial features have also been reported. In rare cases, some newborn infants with Sly syndrome may experience abnormal accumulation of fluid in various tissues of the body (hydrops fetalis). MPS VII is currently in clinical trial.
DiFerrante syndrome (mucopolysaccharidosis VIII; MPS VIII) is an obsolete term for a form of MPS described in a single individual with clinical and biochemical features of Morquio and Sanfilippo syndromes. The disorder had been reported to be due to a deficiency of glucosamine-6-sulfate sulfatase. Subsequently, this disorder was called MPS VIII (DiFerrante syndrome). Dr. DiFerrante later found that the enzyme was normal in his patient, and the disorder had been misdiagnosed. Therefore, DiFerrante syndrome is not a valid medical disorder.
Hyaluronidase deficiency (mucopolysaccharidosis IX; MPS IX) is an extremely rare form of MPS characterized by a deficiency of the enzyme hyaluronidase, which is needed to breakdown the mucopolysaccharides known as hyaluronan (hyaluronic acid). This form of MPS was first described in 1996. Symptoms may include mild short stature, cysts, frequent ear infections, cleft palate, and the development of soft-tissue masses. However, more cases of this form of MPS must be identified before a clear clinical picture can be established. rarediseases.org/rare-diseases/mucopolysaccharidoses/
Sangamo website www.sangamo.com/patients-families/mps-i-ii Hurler syndrome (also known as Mucopolysaccharidosis I, or MPS I) and Hunter syndrome (also known as Mucopolysaccharidosis II, or MPS II) are rare genetic diseases that result in the toxic buildup of complex sugars in the body called glycosaminoglycans, or GAGs. MPS I and MPS II can lead to serious medical problems including early death. Symptoms may not present at birth, but frequently appear in early childhood and may include delayed development, enlarged internal organs, heart conditions, stunted growth, skeletal abnormalities, and joint problems.
MPS I: Three forms of MPS I , in order of increasing severity, include Scheie, Hurler-Scheie, and Hurler Syndromes.
Children born to an MPS I parent carry a defective IDUA gene, which has been mapped to the 4p16.3 site on chromosome 4. The gene is named IDUA because of its iduronidase enzyme protein product. As of 2001, 52 different mutations in the IDUA gene have been shown to cause Hurler syndrome.
Because Hurler syndrome is an autosomal recessive disorder, affected persons have two nonworking copies of the gene. If someone is born with one normal and one defective copy of the gene, (s)he is called a carrier and will produce less α-L-iduronidase than an individual with two normal copies of the gene. The slightly reduced production of the enzyme in carriers, however, remains sufficient for normal function and the person should not show any symptoms of the disease.
MPS II Hunter
1 in 100,000 to 150,000 males are affected by MPS II
Although no studies have been done to determine the frequency of MPS I in the United States, studies in British Columbia estimate that one in 100,000 babies born has severe MPS I. The estimate for attenuated MPS I is one in 500,000 births and one in 115,000 births for individuals whose disease symptoms fall between severe and attenuated
From revenue standpoint, I do not believe MPS I will contribute much (maybe 30-50 million annual opportunity). What is more important is a validation that this technology works in human trials which then will open the floodgates to using gene editing to possibly all kinds of monogenic diseases(and someday possibly diseases caused by multiple genes).
Under: Been on the sidelines for a bit holding (building) cash. Now that "BIGLEY" has rolled out the tax plan its time to jump in.
Dec 21, 2017 19:06:02 GMT -6
martyc: Looks like you are buying Msft again!
Dec 15, 2017 11:23:29 GMT -6
martyc: The news that Trump called Rupert to congratulate him sure seems to indicate that this is heading to approval
Dec 15, 2017 11:22:23 GMT -6
Under: DIS finally getting some traction.?
Dec 14, 2017 17:08:45 GMT -6
martyc: I took an entry level position in DIS. Will add eventually to overweight when it becomes clearer that the deal will go thru. Can't believe how well positioned they will be. 60% Hulu. 20% of content watched on NFLX they can pull. More in thread
Dec 14, 2017 11:05:16 GMT -6
Under: Great posts on $DIS
Dec 13, 2017 17:50:49 GMT -6
Under: $ROKU Citron on a war path.
Nov 28, 2017 15:11:20 GMT -6
Under: $HAS takeover bid for $MAT?
Nov 10, 2017 16:16:07 GMT -6
martyc: Not looking like the market will provide any discounted opp for SGMO. Call was just too professional and all signs indicate they are on a great path for commercialization. Happy with core but wish I had some trading shs
Nov 10, 2017 9:04:05 GMT -6
martyc: For anyone looking to find an entry point into SGMO, I'm almost hoping is sells off in next few days so I can add more. They are really clicking but the fact they haven't signed new deals might cause some to exit. Watching as I have room for trading shs
Nov 9, 2017 18:28:09 GMT -6
martyc: Been an interesting ride so far. I figured the Bears would be about this good but hoped the O wouldn't look so lame. Another building yr but still possible to get to 8-8 IMO
Nov 9, 2017 18:26:08 GMT -6
Under: whats up with your Bears this year Marty?
Nov 9, 2017 17:35:25 GMT -6
martyc: Hope you were long ROKU. I wanted to see Q first so missed out
Nov 9, 2017 7:08:53 GMT -6