The shares of Agios Pharmaceuticals Inc (NASDAQ:AGIO) currently has mean rating of 2.25 while 1 analysts have recommended the shares as “BUY”, 4 recommended as “OUTPERFORM” and 3 recommended as “HOLD”. The rating score is on a scale of 1 to 5 where 1 stands for strong buy and 5 stands for sell.
The company’s mean estimate for sales for the current quarter ending Jun-16 is 39.62 million by 8 analysts. The means estimate of sales for the year ending Dec-16 is 119.80 million by 8 analysts.
The mean price target for the shares of Agios Pharmaceuticals Inc (NASDAQ:AGIO) is at 62.83 while the highest price target suggested by the analysts is 90.00 and low price target is 46.00. The mean price target is calculated keeping in view the consensus of 9 brokerage firms.
The average estimate of EPS for the current fiscal quarter for Agios Pharmaceuticals Inc (NASDAQ:AGIO) stands at -0.48 while the EPS for the current year is fixed at -3.31 by 8 analysts.
The next one year’s EPS estimate is set at -4.93 by 8 analysts while a year ago the analysts suggested the company’s EPS at -3.31.
In its latest quarter ended on 31st March 2016, Agios Pharmaceuticals Inc (NASDAQ:AGIO) reported earnings of -$0.61. The posted earnings topped the analyst’s consensus by $0.18 with the surprise factor of 22.80%. In the matter of earnings surprises, the term “Cockroach Effect” is often implied. Cockroach Effect is a market theory that suggests that when a company reveals bad news to the public, there may be many more related negative events that have yet to be revealed. In the case of earnings surprises, if a company is suggesting a negative earnings surprise it means there are more to come.
On June 11, 2016 Agios Pharmaceuticals Inc (AGIO) announced initial data demonstrating that AG-348 achieved proof-of-concept in an ongoing Phase 2 study (DRIVE-PK) of patients with pyruvate kinase (PK) deficiency, a rare, potentially debilitating, congenital anemia. AG-348 is a novel, first-in-class, oral activator of both wild-type (normal) and mutated pyruvate kinase-R (PKR) enzymes. AG-348 is wholly owned by Agios. Data will be presented today at the 21st Congress of the European Hematology Association (EHA) taking place June 9-12, 2016 in Copenhagen.
DRIVE-PK is the first study to evaluate the safety and efficacy of AG-348 in patients with PK deficiency. As of the March 27, 2016 data cut-off, 18 transfusion-independent patients (13 with at least one missense mutation and five with two non-missense mutations) were treated with twice-daily dosing of AG-348 for up to six months. Treatment resulted in rapid and sustained hemoglobin increases of >1.0 g/dL in nine out of 18 patients (nine of 13 patients with at least one missense mutation), ranging from 2.3–4.9 g/dL with a mean maximum hemoglobin increase of 3.4 g/dL. It is estimated that approximately 80 percent of all PK deficiency patients carry at least one missense mutation. These data support the hypothesis that AG-348 restores metabolic function and has the potential to correct the underlying defect in the red blood cells of patients with PK deficiency.
“People with PK deficiency suffer from chronic anemia and a range of other complications brought on by both their disease and existing supportive therapies, including blood transfusions and splenectomy,” said Rachael Grace, M.D., of the Dana-Farber Boston Children’s Cancer and Blood Disorder Center and a principal investigator for the study. “These data are exciting for the hematology community and patients, as they demonstrate the potential for AG-348 to provide the first disease-modifying treatment with impressive and prolonged increases in hemoglobin levels.”
“These data have established proof-of-concept for AG-348, validating our novel approach to the treatment of rare genetic metabolic disorders by correcting the underlying enzymatic defect with a small molecule,” said Chris Bowden, M.D., chief medical officer at Agios. “The rapid and sustained hemoglobin increases and well-tolerated safety profile shown in this trial to date support continued study and moving into late-stage development. In addition, these data demonstrate the important potential role that PK activation may have in transforming treatment of PK deficiency.”