Target $110
Thursday, July 18, 2019
Danaher Corporation EPS beats by $0.03, beats on revenue
Danaher Corporation (NYSE:DHR): Q2 Non-GAAP EPS of $1.19 beats by $0.03; GAAP EPS of $0.97 beats by $0.02.
Revenue of $5.16B (+3.6% Y/Y) beats by $70M.
UnitedHealth beats Q2 consensus; 2019 guidance raised
UnitedHealth (UNH) Q2 results: Revenues: $60,595M (+8.0%); Premiums: $4,7164M (+6.1%); Products: $8,353M (+19.3%); Services: $4,496M (+5.3%); Investment and other income: $582M (63.9%).
UnitedHealthcare: $48,594M (+5.8%); Optum: $28,029M (+13.4%).
Net Income: $3,293M (+12.7%); EPS: $3.42 (+14.8%); Non-GAAP Net Income: $3,473M (+12.5%); Non-GAAP EPS: $3.60 (+14.6%); CF Ops: $9,108M (-26.4%).
2019 Guidance: GAAP EPS: $13.95 – 14.15 from $13.80 – 14.05; Non-GAAP EPS: $14.70 – 14.90 from $14.50 – 14.75; GAAP net income: $13,500M – 13,750M from $13,425M – 13,750M; Non-GAAP net income: $14,220M – 14,470M from $14,115M – 14,440M.
Shares are up 1% premarket.
Bayer, Bristol-Myers, Ono in Pact on Colorectal Cancer Combo Therapy
- Combination of regorafenib and nivolumab vs. regorafenib alone to be evaluated in patients with micro-satellite stable metastatic colorectal cancer
- Companies plan indication-seeking trial
Bayer, Bristol-Myers Squibb Company (NYSE: BMY) and Ono Pharmaceutical Co., Ltd. (“Ono”) announced today the three companies have entered into a clinical collaboration agreement to evaluate the combination of Bayer’s kinase inhibitor Stivarga®(regorafenib) and Bristol-Myers Squibb’s / Ono’s anti-PD-1 immune checkpoint inhibitor, Opdivo® (nivolumab) in patients with micro-satellite stable metastatic colorectal cancer (MSS mCRC), the most common form of mCRC.1
Regorafenib as monotherapy has demonstrated an overall survival benefit versus placebo in the pivotal Phase III CORRECT study and has shown activity irrespective of micro-satellite status in a retrospective analysis from this study, though with limited responses observed.2,3 Despite progress in the treatment of CRC, including the advance of effective immuno-oncology (I-O) treatments for certain subsets of CRC, around 95% of mCRC patients have MSS tumors, for which I-O monotherapy treatment approaches have shown limited activity.4 Thus, the need for additional treatment options including combination approaches remains high.4 Encouraging early data have been seen with the combination of regorafenib and nivolumab. In a Phase 1b investigator sponsored trial from Japan called REGONIVO (NCT03406871, EPOC1603), the combination of regorafenib and nivolumab has shown promising preliminary efficacy results.1 The detailed data of the study were presented at the 2019 American Society of Clinical Oncology (ASCO) Annual Meeting.
“The data seen in REGONIVO warrant further exploration of the combination of regorafenib and nivolumab in patients with colorectal cancer. Regorafenib has proven its efficacy and positive safety profile as a third-line monotherapy and we are excited to enter into a clinical collaboration to evaluate this combination with the hope to deliver an additional therapeutic benefit to patients,” said Scott Z. Fields, M.D., senior vice president and head of Oncology Development at Bayer’s Pharmaceuticals Division.
“We continue to invest in innovative approaches to maximize the potential of our pipeline, and interrogate new combinations to help more patients with cancers typically not responsive to I-O therapy,” said Fouad Namouni, M.D., head of development, oncology, Bristol-Myers Squibb. “We are looking forward to a strong collaboration to investigate nivolumab with regorafenib, with the goal of serving more patients who have cancer.”
“We have been actively engaged in the development of nivolumab including combination therapies with other agents. We are excited to initiate the clinical collaboration with Bayer and Bristol-Myers Squibb to investigate this combination therapy as a new treatment option for patients with colorectal cancer and other types of cancer,” said Kiyoaki Idemitsu, Corporate Officer, Executive Director, Clinical Development, Ono.
Eli Lilly, AC Immune Start Phase 1 Study of Investigational Alzheimer’s Treatment
AC Immune SA (NASDAQ: ACIU), a Swiss-based, clinical-stage biopharmaceutical company, today announced dosing of the first subject in a Phase 1 study of ACI-3024, a first-in-class investigational oral small molecule Tau Morphomer inhibitor that will be studied in neurodegenerative diseases that are characterized by the presence of pathological Tau aggregates.
This is the first significant advancement in AC Immune’s collaboration with Eli Lilly and Company (NYSE:LLY).
Prof. Andrea Pfeifer, CEO of AC Immune SA, commented: ‘The start of this study is an important milestone for AC Immune in our collaboration with Lilly for patients suffering from debilitating neurodegenerative diseases. It demonstrates the productivity of our proprietary small molecule Morphomer discovery platform and further expands our robust clinical pipeline to address neurodegenerative diseases, in particular for therapeutics and diagnostics targeting Tau. Addressing Tau pathology with precision medicine is a key therapeutic strategy for Alzheimer’s disease (AD) and other neurodegenerative diseases.’
ACI-3024 is the primary focus of a license and collaboration agreement between AC Immune and Lilly to research and develop small molecule Tau aggregation inhibitors for the treatment of AD and other neurodegenerative diseases. The collaboration combines AC Immune’s proprietary Morphomer discovery platform and early development experience with Lilly’s established clinical development expertise and commercial capabilities in central nervous system disorders. AC Immune will conduct the initial Phase 1 development of the Morphomer Tau aggregation inhibitors while Lilly will fund and conduct further clinical development.
The Phase 1 trial is a randomized, placebo controlled, double blind, sequential single and multiple ascending dose study with open label food effect and pharmacodynamics assessment arms to assess the safety, tolerability, pharmacokinetics, and pharmacodynamics of ACI-3024 in healthy volunteers.
Dr. Sonia Poli, Vice President Translational Science and Project Leader of AC Immune SA, commented: ‘In the complex treatment paradigm for AD, Tau pathology is a potential therapeutic target because Tau spreads with a characteristic spatiotemporal pattern throughout the brain that coincides with both clinical symptoms and disease progression in AD. Slowing the propagation of Tau pathology may slow disease progression and reduce cognitive decline. Anti-Tau therapies already have shown promise in slowing the progression of Tau pathology in animal models.’
Eisai Presents Nonclinical Research Results of Elenbecestat at AAIC 2019
Eisai Co.,Ltd. announced its latest data of nonclinical research which examined the effect to the synaptic function in the brain by spinal densities(1) in regard to oral BACE (beta-site amyloid precursor protein cleaving enzyme) inhibitor elenbecestat(2) were presented at the Alzheimer’s Association International Conference (AAIC) held in Los Angeles, California, United States, from July 14 to 18, 2019 (Poster Presentation No.: P2-064).
BACE is a key enzyme in the production of Abeta peptides, which inhibits beta site of amyloid precursor protein (APP). BACE inhibitor may decrease the formation of toxic Abeta peptide aggregates in the brain, thereby thought to exert disease modifying effects and may have potential to slow the disease progression. On the other hand, in addition to APP, the other substrates with physiological role in synapse formation and function are known as a substance (substrate) changed by BACE.
At this time, the effect to Abeta level in CSF and synaptic damage were examined after 4 weeks of administration of BACE inhibitors using novel preclinical model mouse. For the examination compounds, elenbecestat (in-house discovery), verubecestat, and lanabecestat were used.
In addition, the effect to the synapse formation and function were evaluated by setting the numerous spinal densities on dendrite of brain cortex (number of spines per 10 micrometer of dendrites) and mitochondrial function (mitochondrial oxygen efficiency) of hippocampal synaptosomes (isolated presynaptic terminal) as an index. It is believed that decreases in spinal densities and mitochondrial function damage the synaptic function and deteriorate the cognitive function.
The dose of each BASE inhibitor was adjusted so as to be equivalent to the dose for clinical study in accordance with exploratory data of lowering effect of Abeta in mouse CSF. As a result, elenbecestat did not show significant effects on spinal density and mitochondrial function at dose of 3, 10mg/kg with significant decline of Abeta level in CSF (p<0.001).
As for the verubecestat, significant decline of spinal density was shown at the dose of 10, 30mg/kg (p<0.05) with significant decline of Abeta level in CSF (p<0.001).
Also, as for lanabecestat, significant decline of spinal density was shown at the dose of 30, 100mg/kg (p<0.05) with the significant decline of Abeta level in CSF (p<0.001), as well as the significant decline of mitochondrial function was shown at the dose of 100mg/kg (p<0.05).
These results suggest that elenbecestat does not affect the synaptic function in the brain with an effective dose to decline the Abeta level in CSF.
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