Ocera Therapeutics, Inc.
Ocera Therapeutics, Inc. (Form: 8-K, Received: 01/09/2017 09:04:54)

UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
Washington, D.C. 20549

FORM 8-K
CURRENT REPORT
Pursuant to Section 13 or 15(d) of The Securities Exchange Act of 1934
Date of Report (Date of Earliest Event Reported): January 5, 2017
OCERA THERAPEUTICS, INC.
(Exact name of registrant as specified in its charter)
 
 
 
 
 
 
DELAWARE
 
001-35119
 
63-1192270
(State or other jurisdiction
 
(Commission File Number)
 
(I.R.S. Employer
of
 
 
 
Identification No.)
incorporation)
 
 
 
 
Registrant’s telephone number, including area code (650) 475-0150
 
 
 
 
525 University Avenue, Suite 610
 
 
Palo Alto, CA
 
94301
(Address of principal executive offices)
 
(Zip Code)
Not Applicable
(Former name or former address, if changed since last report)
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:
o      Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)
o      Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)
o      Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))
o      Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))




Item 7.01.  Other Events.
The management of Ocera Therapeutics, Inc. (the “Company”) will participate in investor meetings at the 35th Annual J.P. Morgan Healthcare Conference beginning on Monday, January 9, 2017 in San Francisco. A copy of the presentation slide deck to be used in conjunction with the investor meetings is being furnished as Exhibit 99.1 to this Report on Form 8-K.
The information in this Item 7.01 and Exhibit 99.1 attached hereto is intended to be furnished and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the “Exchange Act”) or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as expressly set forth by specific reference in such filing.
Item 8.01 Other Events.
On January 5, 2017, the Company issued a press release announcing the results of its Phase 1 clinical study of orally-administered OCR-002 in patients with cirrhosis. The full text of the press release is filed as Exhibit 99.2 to this Current Report on Form 8-K and is incorporated herein by reference.
Item 9.01. Financial Statements and Exhibits.
(d) Exhibits
Exhibit No.
 
Description
99.1
 
Ocera Therapeutics, Inc. Presentation Slide Deck.
99.2
 
Press release issued by Ocera Therapeutics, Inc. dated January 5, 2017.





SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
 
 
 
 
 
January 9, 2017
 
Ocera Therapeutics, Inc.
 
 
 
 
 
By:
/s/ Linda S. Grais, M.D.
 
 
Name: Linda S. Grais, M.D.
 
 
Title: President and Chief Executive Officer





EXHIBIT INDEX
Exhibit No.
 
Description
99.1
 
Ocera Therapeutics, Inc. Presentation Slide Deck.
99.2
 
Press release issued by Ocera Therapeutics, Inc. dated January 5, 2017.


A Liver Disease Medicines Company NASDAQ: OCRX J A N UA R Y   2 0 1 7


 
2 Forward‐Looking Statements Certain statements in this presentation constitute “forward‐looking statements” within the meaning of  the Securities Act of 1933, as amended (the “Securities Act”), and Securities Exchange Act of 1934, as  amended (“Exchange Act”), including, without limitation, all statements related to the OCR‐002 clinical  development program, including patient enrollment estimates, expected timing for the receipt of clinical  data, the potential success of OCR‐002 in clinical trials, the size of the potential market opportunity for  OCR‐002, as well as cash projections, and we intend these forward‐looking statements to be covered by  the safe harbor provisions for forward‐looking statements contained in the Securities Act and the  Exchange Act and are making this statement for purposes of complying with those safe harbor provisions.  These forward‐looking statements reflect our current views about our plans, intentions, expectations,  strategies and prospects, which are based on the information currently available to us and on  assumptions we have made. Although we believe that our plans, intentions, expectations, strategies and  prospects as reflected in or suggested by those forward‐looking statements are reasonable, we can give  no assurance that the plans, intentions, expectations or strategies will be attained or achieved.  Furthermore, actual results may differ materially from those described in the forward‐looking statements  and will be affected by a variety of risks and factors that are beyond our control, including those risks and  uncertainties discussed under “Risk Factors” in our Annual Report on form 10‐K for the year ended  December 31, 2015, as well as other risks detailed in our subsequent filings with the SEC. All information  in this presentation is as of the date of this presentation, and we undertake no duty to update this  information unless required by law.


 
3 Seeking to Provide Continuity of Care from Treatment to Prevention Developing Therapeutics for  Liver Diseases Lead Program OCR‐002 Ammonia Scavenger for Hepatic Encephalopathy (HE)  IV‐Phase 2b ACUTE Oral‐Phase 1 CHRONIC


 
4 Investment Highlights  OCR‐002 for Hepatic Encephalopathy (HE): ~$1.5‐2B potential U.S.  market opportunity  Novel ammonia scavenger; broad IP protection & WW rights  IV formulation for acute use and oral formulation for chronic use  Only direct ammonia scavenger in development for HE DIFFERENTIATED  PRODUCT FOR  UNMET NEED  IV Phase 2b STOP‐HE study data  Oral Phase 2a multi‐dose study initiation in cirrhotic patients ANTICIPATED  NEWS FLOW  NEXT TWO  QUARTERS  Cash as of September 30, 2016: $32.5M  Existing cash resources expected to fund development into Q1 2018 FINANCIAL  STRENGTH


 
5 LINDA S. GRAIS, MD, JD President & Chief Executive Officer STAN BUKOFZER, MD Chief Medical Officer MICHAEL BYRNES, MBA Chief Financial Officer Experienced Leadership AND a Team with Deep Clinical and Development Experience


 
6 Disorientation Impaired  Motor Skills Personality Changes Stupor Coma Death 0 1 2 3 4 Hepatic Encephalopathy (HE):  Neurocognitive Disorder in Serious Liver Disease Blood Stream Ammonia Gut Elevated Ammonia Levels Drive HE Note: 0 to 4 as measured by West Haven Scale


 
7 OCR‐002 Mechanism of Action: Clears Ammonia When the Liver Cannot Ornithine Contributes to Glutamate, which combines with Ammonia to Create Glutamine Gut OCR- 002 Kidney PAGN Excretion AmmoniaGlutamate PAA Combines with Glutamine to Form Phenylacetylglutamine (PAGN) Which Is Excreted Through Kidneys Phenylacetic Acid (PAA) Non-Toxic Carrier of Ammonia, Contributes to Muscle Building Glutamine PAGN Note: Simplification of MOA


 
8 Ammonia Lowering Reduced Risk of HE in  HALT‐HE Study 1 “Randomized, Double‐Blind, Controlled Study of Glycerol Phenylbutrate in Hepatic Encephalopathy” Rockey, et al. Hepatology 2014; 59:1073‐1083 2 “Fasting Ammonia (NH3) as a Predictor or Hepatic Encephalopathy (HE) Events” Vierling, et al. Journal of Hepatology 2013; 58: S63‐S227 • Studies have long observed an  association between ammonia and HE • Causal link demonstrated by Ravicti®  HALT‐HE Study – Significantly delayed time to next HE  episode (p<0.05)1 – Significantly reduced proportion of  patients who experienced HE episode  (p=0.02)1 – Patients with baseline fasting ammonia  >1.5x upper limit of normal had a six‐ fold elevation in rate of annualized HE  episodes compared to patients with  fasting ammonia between 0‐1.5x ULN  (p<0.01)2


 
9 OCR‐002 is the ONLY Direct Ammonia Scavenger in  Development for HE Treatment and Prevention Ammonia RIFAXIMIN Non‐Absorbed Antibiotic  Kills Gut Bacteria − Only approved for maintenance,  not acute treatment − Does not directly clear circulating  ammonia LACTULOSE Laxative, Used for Decades + Inexpensive − Hard to administer − Diarrhea − Poor compliance Current  Treatments are  Indirect and  Limited to Oral RAVICTI Active Ingredient: Phenylacetate + Ammonia scavenger approved for UCD + Strong clinical efficacy for HE prevention − HE development halted by Horizon − Priced for genetic ultra‐orphan disease,  unsuitable for HE AMMONUL Sodium Phenylacetate and Sodium Benzoate + Potent in acute urea cycle disorders − Requires large volumes − Label cautions usage due to high sodium  load; electrolyte and fluid shifts may be  unsafe in HE patients Other  Ammonia Scavengers  Not Approved for HE


 
10 OCR‐002 Designed to Treat HE • IV easy to administer in acute care patients – Peripheral IV line, low infusion volume and neutral pH  – Rapid onset  – Demonstrated favorable safety and tolerability profile in sick  population – No sodium load or electrolyte disturbances • Oral formulation for chronic care patients – PAA validated ammonia scavenger in HALT‐HE Study for  prevention of HE – Provides continuity of care for patients at home – Provides opportunity for step‐down care post IV therapy


 
11 • Sample size of approximately 230 patients provides 80% power to detect the difference at study‐end that  was observed at the planned interim analysis STOP‐HE Phase 2b: OCR‐002 IV for Overt HE Enrollment Complete – Data Q1 2017 *As scored by a modified version of the West Haven Scale Key Exclusion • Kidney failure/dialysis • Life expectancy < 2 weeks HOSPITALIZED  CIRRHOTICS Key Inclusion • West Haven* Score ≥ 2 • Ammonia >ULN • Standard of care (SOC)  treatment and observation • Physician’s choice for SOC • Patients must remain in   HE  • Weed out rapid  responders MINIMUM 12‐HOUR PRE‐SCREEN • Randomized 1:1  − placebo + SOC − drug +  SOC • Continuous infusion for up  to 5 days • Patient assessed 2x/day • Primary Endpoint: Time to  meaningful clinical  improvement in HE  symptoms TREATMENT


 
12 • Primary Endpoint: Time to meaningful clinical improvement in HE symptoms • Secondary Endpoints: Time to complete resolution of HE symptoms, % responders, length of hospital stay • Exploratory endpoints: Ammonia interrelationships, hospital discharge destination Meaningful Clinical Improvement = Event As Scored by Modified Version of West Haven Scale Stage / Symptoms Meaningful Clinical Improvement 4 to 2 or  lower 3 to 2 or  lower 2 to 1  or  lower 0 1 2 3 4 ‐ ‐ ‐ H o s p i t a l i z a t i o n   ‐ ‐ ‐Comatose Stuporous Disoriented Difficult to Arouse Asterixis Mild Confusion Normal M o d e r a t e M i l d S e v e r e


 
13 STOP‐HE Study Powering Assumptions Initial Design Following DMC  Recommendation  At Interim Analysis PBO Active PBO Active Percent Response thru  5 days (120 hrs) 45% 65% ? ? Median Time to  Response  5.7 days (139 hrs) 3.2 days (79 hrs) ? ? Treatment Benefit 2.5 days (60 hrs)* Observed by DMC Total Patients 200 ~230 Power 80% 80% • 200 patients is 80% powered to show treatment benefit of 60 hours • 230 patients is 80% powered to show treatment benefit at the end of the study  that was observed by the DMC at the interim analysis *Any Treatment Benefit in Excess of 24 hours is Considered Meaningful


 
14 STUDY RAVICTI® Phase 2 HALT‐HE OCR‐002 STOP‐HE (Enrollment Complete) Dose of Drug 6mL BID = 13.2g/day 10g/15g/20g/day  (depending on liver function, dose  adjustment to normalize PAA levels) Mean PAA  Exposure 65‐150μg/mL1 Target: 75‐150μg/mL Clinical  Results Statistically significant reductions in  incidence of HE events and time to first  event2 Promising interim analysis; sample size  recommendation highly suggestive of  treatment benefit  Conclusion Dose sufficient for clinical benefit Dosing strategy to achieve similar PAA  levels as RAVICTI® study   1 “Glycerol Phenylbutyrate in Patients With Cirrhosis and Episodic Hepatic Encephalopathy: A Pilot Study of Safety and Effect on Venous Ammonia Concentration” Ghabril, et al. Clinical Pharmacology in Drug Development 2013; 2(3) 278‐284 2 “Randomized, Double‐Blind, Controlled Study of Glycerol Phenylbutrate in Hepatic Encephalopathy” Rockey, et al. Hepatology 2014; 59:1073‐1083 Dose Rationale for OCR‐002 Informed by HALT‐HE


 
15 Outlook for STOP‐HE Favorable  Safety and  Tolerability  Profile PROMISING FACTORS Appropriate  Dosing Level Clinically  Validated  Mechanism Encouraging Interim  Analysis Enrollment Completed; Data Expected Q1 2017


 
16 Oral OCR‐002 Unique Opportunity  Develop orally‐administered formulation of OCR‐002 in concert  with IV formulation to provide continuity of care for HE patients GOAL OF OCR‐002  ORAL PROGRAM  Phase 1 program showed favorable single‐dose PK data  Phase 2a study with new optimized tablet formulation planned  for H1 2017 STATUS AND  NEXT STEPS  1.5‐2M cirrhotics at risk of hepatic encephalopathy in the U.S.  Less than 10% of at risk population represents $900M ‐ $1.2B  potential revenue opportunity in the U.S. alone  High re‐hospitalization rate for those discharged MARKET  OPPORTUNITY


 
17 Proof of Principle Achieved in Phase 1 Program Phase 1: Cirrhotic Patient Study – Completed Q1 17 Single Dose Orally‐Administered OCR‐002 Findings include: Single IV Dose of OCR‐002VS • Absolute bioavailability > 95% in the fasted state • Pharmacokinetics supporting convenient dosing Extended‐Release Formulations of OCR‐002 Glycerol Phenylbutyrate (RAVICTI®) Immediate‐Release Oral Solution of OCR‐002 VS Phase 1: Healthy Volunteer Study – Completed Q4 15 Findings include: • Rapid onset of adequate plasma PAA concentrations with all OCR‐002 formulations • Sustained higher drug levels and PAGN than Ravicti All doses and treatment arms of OCR‐002 observed were safe and well‐tolerated


 
18 Oral OCR‐002 Phase 2a Study; Initiation H1 2017 Multi‐Dose Orally‐Administered OCR‐002 Glycerol Phenylbutyrate (RAVICTI®)VS Phase 2a: Cirrhotic Patients Evaluation of: • New optimized tablet formulation of OCR‐002 • Steady state pharmacokinetics • Pharmacodynamics • OCR‐002 vs. Clinically‐validated ammonia scavenger


 
19 Ammonia Brain Swelling3 Portal  Hypertension2 NASH4 Protein  Catabolism5 Neuronal Cell Death1 Elevated Ammonia Correlated with Other Complications  of Cirrhosis; OCR‐002 Potentially Beneficial 1 Oral Presentation; Clément et al (AASLD 2015) 2 Jalan, et al “Ammonia produces pathological changes in human hepatic  stellate cells and is a target for therapy of portal hypertension” J Hepatology  2016 p. 823‐233 3 Oral Presentation; Ventura‐Cots et al (AASLD 2015) 4 Poster #908; Thomsen et al (AASLD 2015) 5 Poster #1523; Bosoi et al (AASLD 2015)


 
20 Addressing a Serious Problem  Multiple Causes of Liver Disease (U.S.) CHRONIC LIVER DISEASE 30‐35M1 LIVER CIRRHOSIS 5.5M Million2 AT RISK OF OHE ~1.5‐2M3 ~200K Patients with OHE4 1 American Liver Foundation, Clinical Gastroenterology and Hepatology, 2011;9:524‐530 Zobair et al 2 Clin Liver Dis (2012) 73‐89 Khungar et al 3 Hepatology August 2014 AASLD guideline, Annual risk for development 20% (Clin Gastroenterol Hepatol 201 November, Bajaj) 4 HCUP, Company estimate


 
21 1 HCUP Database 2 Clinical Gastroenterology and Hepatology 2012;10:1034–1041 3 Annualized based off of actual reported revenues from Q1‐16 through Q3‐16 HE: Large and Growing Healthcare Burden Rising Hospitalizations1 (000s) • Total national charges  related to HE: $7 Billion2 • HE hospitalizations  continue to grow despite  Rifaximin launch in 20101 • Rifaximin annual revenues:  $900+ Million3 • HE patient demographics  show increase in severity  of illness, elderly  population, and obesity as  comorbidities2 105 107 106 110 120 133 141 148 156 83 104 180 196 252 275 331 380 436 2006 2007 2008 2009 2010 2011 2012 2013 2014 Hepatic Coma Encephalopathy Rifaximin  approved for  Prevention of  HE April 2010


 
22 Long Patient Stays1 HE Patient Distribution 60% >4days >14 days 15% 5‐14 days 45% 1‐4 days 40% Faster Improvement in HE Can Reduce Length of Stay 1 Ocera market research (CMS Medicare U.S. data 2011) 2 Becker’s Review / Hospital Review / May 2015 3 HCUP Hospital Intensive Care Units 2011 • ~One third of HE patients are treated in ICU1 ‐ Average in‐patient hospital bed “cost” is  $1,500‐$2,000/Day2 ‐ ICU cost approximately ~2.5X3 • 45‐50% of hospitalized HE patients are on  Medicare1 ‐ Hospitals start losing money around day  four Hospital Cost Drivers Hospital stay/ICU stay and Medicare HE: Longer Hospitalization Drives Cost


 
23 • Seeks to provide continuity of  care with IV • Goal is to prevent re‐ hospitalization and enable  patients to remain stable at  home ORAL • Up to 600K annual  hospitalizations1 • Potentially favorable   reimbursement • $1,300 / day for OCR‐0022 • Presumed standard of care • Protocol in most institutions  IV Significant Commercial Opportunity for IV and Oral OCR‐002 $600 ‐ 800MM $900 ‐ 1.2MM ~200K PAT I E N T S   A NNUA L LY ~$1.5‐2B U. S .   O P PORTUN I T Y 1 HCUP Database (includes ICD‐9 codes 572.2/hepatic coma and 348.3/ encephalopathy NOS) 2 Company research 


 
24 Valuable Commercial Estate  BROAD PATENTS Composition  of Matter to 2030 (not including  Hatch‐Waxman  extension) ORPHAN STATUS IN US WORLDWIDE RIGHTS


 
25 HIGH HE Burden UNMET Medical Need ONLY Direct Ammonia Scavenger for HE PROMISING Clinical Programs ATTRACTIVE Commercial Opportunity NEAR TERM MILESTONES • STOP‐HE P2b Data • Oral P2a Multi‐dose Study Initiation V11022016


 
OCERAANNOUNCESSUCCESS_IMAGE1.JPG


Exhibit 99.2
PRESS RELEASE


Ocera Announces Successful Phase 1 Clinical Study of Orally-Administered
OCR-002 in Patients with Cirrhosis

Data Support Feasibility of Oral OCR-002 as Maintenance Therapy for Patients with Hepatic Encephalopathy

Company Plans to Initiate Phase 2a in H1 2017 with New Optimized Tablet Formulation

PALO ALTO, Calif. and RESEARCH TRIANGLE PARK, N.C., January 5, 2017 – Ocera Therapeutics, Inc. (NASDAQ:OCRX), today announced positive results from a Phase 1 clinical study of orally-administered OCR-002 (ornithine phenylacetate) in patients with cirrhosis. The Company is developing oral OCR-002 for chronic use to maintain remission of hepatic encephalopathy (HE), a neurocognitive disorder associated with serious liver disease.

“We are excited to report the findings showed favorable oral absorption and pharmacokinetics in the intended population,” said Stan Bukofzer, M.D., Chief Medical Officer of Ocera. “This was the first study in which OCR-002 was delivered orally to patients with cirrhosis. We believe these data support our plan to study the administration of OCR-002 orally and chronically to patients with cirrhosis with the goal of keeping them stable in the outpatient setting.”

In light of the insight gleaned from these results, Ocera plans to conduct a multi-dose Phase 2a study in cirrhotic patients using a tablet formulation to determine the steady-state PK and pharmacodynamics of OCR-002 over a range of doses. The Phase 1 study announced today used a liquid formulation. The Company expects to initiate the Phase 2a study in the first half of 2017.

Summary of Key Findings:
OCR-002 was observed to be safe and well-tolerated across all treatment arms in the study.
OCR-002 demonstrated absolute oral bioavailability of greater than 95% in the fasted state.
Dosing under fed conditions delayed absorption slightly, lowered mean maximum concentration (Cmax) by 30-40% and reduced the absolute oral bioavailability to 75-80%. These data suggest the drug is potentially suitable to be taken conveniently at mealtime corresponding with when ammonia levels typically begin to rise in patients with HE.
Plasma levels of the study drug and PAGN were similar when OCR-002 was dosed before and after the discontinuation of lactulose, a current standard of care for HE patients, indicating the study drug may be unaffected by its concomitant use. PAGN is the





molecule formed from the combination of study drug with serum ammonia, and is excreted through the kidneys.
Overall mean plasma exposure to study drug (AUC0-inf) was approximately 35-40% higher in Child-Pugh 1 C patients compared to Child-Pugh A patients, as expected given the greater impairment of liver function of Child-Pugh C patients. The Company believes that the higher plasma exposure is due to lower metabolism of the study drug by the severely impaired livers.

About the Phase 1 Orally-Available OCR-002 Study
The Phase 1 trial was an open-label, crossover study to determine the pharmacokinetics and the absolute oral bioavailability of OCR-002 in patients with varying degrees of cirrhosis. The study evaluated a single 5g dose of IV OCR-002, and single 5g doses of a liquid oral solution of OCR-002 administered across three treatment arms:
Fasted while on lactulose
Fed while on lactulose
Fasted with discontinuation of lactose

About Hepatic Encephalopathy
Hepatic encephalopathy is a debilitating and progressive complication of liver cirrhosis or liver failure, marked by mental changes including confusion, impaired motor skills, disorientation, and in its more severe form, stupor, coma and even death.

About Ocera
Ocera Therapeutics, Inc. is a clinical stage biopharmaceutical company focused on the development and commercialization of OCR-002 (ornithine phenylacetate) in both intravenous and oral formulations. OCR-002 is an ammonia scavenger and has been granted orphan drug designation and Fast Track status by the U.S. Food and Drug Administration (FDA) for the treatment of hyperammonemia and resultant hepatic encephalopathy (HE) in patients with acute liver failure and acute-on-chronic liver disease.

Ocera's HE clinical development efforts also include a recently completed Phase 2b clinical trial, STOP-HE, which evaluated the safety and efficacy of intravenously-administered OCR-002 in resolving neurocognitive symptoms of acute HE in hospitalized patients with elevated ammonia. Enrollment for the Phase 2b intravenous study was completed in December 2016, and the Company expects to publish top-line data of the STOP-HE study in the first quarter of 2017. For additional information, please see www.ocerainc.com.

Forward-Looking Statements
This press release contains "forward-looking" statements, including, without limitation, all statements related to the OCR-002 clinical development program, including but not limited to the potential benefits of OCR-002 to help patients with hepatic encephalopathy, the timing of clinical





and enrollment milestones, and the timing of our clinical development plans and release of study data. Any statements contained in this press release that are not statements of historical fact may be deemed to be forward-looking statements. Words such as "believe," "expected," "hope," "plan," "potential," "will" and similar expressions are intended to identify forward-looking statements. These forward-looking statements are based upon Ocera's current expectations. Forward-looking statements involve risks and uncertainties and Ocera's actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of these risks and uncertainties, including those risks and uncertainties discussed under the heading "Risk Factors" in Ocera's Annual Report on Form 10-K for the year ended December 31, 2015 and subsequent filings with the SEC. All information in this press release is as of the date of the release, and Ocera undertakes no duty to update this information unless required by law.

1 Child-Pugh Scoring is a clinically relevant method of assessing the severity of liver impairment in patients with cirrhosis. A score, ranging from 5 (least severe) to 15 (most severe), is calculated by totaling the scores of five discrete variables: serum bilirubin, serum albumin, prothrombin time, ascites and encephalopathy. Scores of 5-6 are classified as Child-Pugh A (well compensated disease); scores of 10-15 are classified as Child-Pugh B (disease with significant functional compromise); and scores of 10-15 are classified as Child-Pugh C (decompensated liver disease).

###

Source: Ocera Therapeutics, Inc.
OCRX-G

Susan Sharpe
Ocera Therapeutics, Inc.
contact@ocerainc.com 
919-328-1109