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Latest News (September 5, 2016)


Ulcerative Colitis/Crohn’s Disease TLP #21-2016-09 is the 21st iteration of our Gastroenterology Thought Leader Panel dating back to 2003.  This report summarizes thought leader interviews that were conducted in July and August 2016.  For this panel, BOLT International / MedPredict spoke with 6 internationally recognized experts in the treatment of inflammatory bowel disease.  The purpose of this Panel was to identify the events that will reshape the IBD landscape in 2016/2017.  Thought Leaders offered their perspectives on the significance of the approval of vedolizumab for Crohn’s and ulcerative colitis, TNF biosimilars, next-generation anti-integrins, JAK inhibitors, IL23 inhibitors, S1P agonists, SMAD7 inhibitors, stem cells and a variety of therapeutic approaches that are in earlier clinical / preclinical development.  In addition, this Panel spent considerable time on assessing unmet medical needs in IBD.

Discussion Guide

Gastro Discussion Guide 2016-09

To my Panel:  This is a VERY full agenda.  Please feel free to “jump around” in the discussion guide.  Let’s focus on the points that are MOST interesting to you.  Let’s not get distracted with the less important molecules that are being developed to treat ulcerative colitis or Crohn’s disease.

Thoughts on unmet needs: ileal disease, mucosal healing, fistula healing, anything else???

The outcome of the mongersen endoscopy Phase I study.  Did Celgene see clear improvement and that gave the go for Ph 3, or did they start Ph 3 at risk (Clinicaltrials.gov NCT02367183 This study is design to explore the effect of GED-0301 on clinical and endoscopic outcome and to evaluate its safety in subjects with active Crohn’s disease).

It is interesting that tofa did not work in CD, but apparently there is a clear signal for filgotinib.  Can you speak to any difference study design that might be the reason for the different outcome?  Or is filgotinib actually a better JAK?  Will Pfizer try once again with tofacitinib?  Maybe they need to screen for disease by endoscopy?
TD-1473 is a GI-targeted pan-JAK inhibitor that has demonstrated a high affinity for each of the JAK family of enzymes (JAK1, JAK2, JAK3 and TYK2). TD-1473 is specifically designed to distribute adequately and exclusively to the tissues of the GI tract and to minimize systemic exposure.  Compared to the plasma exposure of tofacitinib at twice daily doses of 10 mg, the plasma exposures of TD-1473 at daily doses of 30 mg and 100 mg were about 75-fold and 15-fold lower.  Starting Ph-Ib in UC.
Theravance Biopharma stock symbol TBPA

Etrolizumab, what plans to be the differentiation from vedo?  Will they be developing a diagnostic for patients with high alpha E expression?
Shire licensed Pfizer’s anti-MAdCAM-1, PF-00547659 for moderate-severe IBD.  Did Pfizer decide to focus on TOFA?  Did Pfizer decide that IBD is too small or specialized for them?  How does MAdCAM-1 inhibition compare (efficacy/safety/convenience) to vedolizumab or etrolizumab?

Effi-7 (OSE Immunotherapeutics)  interleukin-7 (IL-7) receptor agonist MAb  “IL-7 receptor blockade prevents intestinal human T cells infiltration by modulation of alpha4-beta7 integrin expression.“  Preclinical poster.  Appears to be another competitor to vedolizumab and friends.

BI sold the rights to AbbVie for risankizumab anti-IL23.  Ph-II reported at DDW 2016: Pts with active Crohn’s disease were randomly treated for 12 weeks either with placebo or risankizumab. After 12 weeks, 24% of patients treated with 200 mg of risankizumab, and 37% treated with 600 mg were symptom free and in remission.  Under endoscopic examination to evaluate deep remission, the rates were 15% for doses of 200 mg risankizumab; 20% among those who received 600 mg of the drug.  Please put these results into context for me, particularly in relation to the ustekinumab data that is available.  Ustekinumab will win the race to get the label.  What must AbbVie show in Crohn’s?  In UC???

“Part two” of this question is how does Janssen position ustekinumab (anti-IL12/IL23) and golimumab (anti-TNF) to maximize the value of their franchise?

Celgene acquired Receptos following the movement of once-daily oral S1P ozanimod into Ph-III registration trials for ulcerative colitis (TRUE NORTH; NCT02435992) and multiple sclerosis (RADIANCE).  The MS trial should report in 2017.  TRUE NORTH should report in 2018.  A Ph-II CD trial is to begin in 2015.  Has there been any interim data?

NKG2D (Janssen / Novo Nordisk) targets NK cells.  These are early responders in the immune system and thus inhibiting them may produce a faster efficacy response than with the anti-adhesion molecules.  One of the biomarkers for efficacy of the JAK inhibitors is a depletion of NK cells.  A theoretical concern is that depletion will translate into an increased infection risk.  This will be the primary concern until/unless long term data allays it.  Is there any clinical data to shed light on this question?

Inflectra (Celltrion): In patients who are anti-TNF naive, who is NOT going to receive biosimilar infliximab?  What about in patients who have received only adalimumab as anti-TNF therapy?

Please only discuss the following if you believe that this is going to be paradigm changing:  RedHill Biopharma: RHB-104 active components (antibiotics clarithromycin, clofazimine and rifabutin).  The association of Mycobacterium
avium subspecies paratuberculosis
(M. paratuberculosis) with Crohn’s disease is a controversial issue.  A significant association was found between  M.paratuberculosis and Crohn’s disease (p = 0.02) that was not related to age, gender, place of birth, smoking or alcohol intake. No significant association was detected between M.paratuberculosis and UC or aphthous ulcers; Timms et. al:

FINALLY: Is there any particular clinical stage molecule that I should have asked about but failed to mention?  Anything of great significance that I am missing?

Ulcerative Colitis / Crohn’s
Thought Leader Panel #21 2016-09

 is available immediately by electronic download.
If you are pharma, please contact Jeff Berk jeff@boltinternational.com for pricing for this report.
If you are a patient, please have your physician contact us for a free copy of this report.  We do not distribute directly to patients.

Contact Jeff Berk at jeff@boltinternational.com for more information.



Latest News (November 2, 2015)





Ulcerative Colitis/Crohn’s TLP #20 2015-11 summarizes a series of thought leader interviews that were conducted in October 2015. For this panel, BOLT / MedPredict spoke with 6 internationally recognized experts in the treatment of inflammatory bowel disease. The purpose of this Panel was to identify the events that will reshape the IBD landscape in 2016/2017. Thought Leaders offered their perspectives on the significance of the approval of vedolizumab for Crohn’s and ulcerative colitis, TNF biosimilars, next-generation anti-integrins, JAK inhibitors, IL23 inhibitors, S1P agonists, SMAD7 inhibitors, IL-6 inhibitors and a variety of therapeutic approaches that are in earlier clinical / preclinical development.


The Panel offers insight in the following areas:


  • Anti-TNF positioning and sequencing in light of the vedolizumab approval.
  • IL-23 +/- IL-12: Stelara in treatment experienced Crohn’s. Role for IL-23 selective inhibitors.
  • JAK: Xeljanz infection risk in IBD.
  • Other Mechanisms
  • SMAD7
  • S1P
  • NK inhibition
  • IL-6
  • IL22
  • TLR-9
  • GPR84
  • IL10
  • ATPase
  • Stem Cells
  • RORγt
  • other


The Panel specifically elaborates on the following Key Findings:


  • The IBD category will see two new approvals in 2016.


  • Ustekinumab will garner an approval in the US and EU for Crohn’s disease, with ulcerative colitis following about a year later. The drug will be available in both an infusion for induction and, if the physician and patient desire, an injection for maintenance.


  • Tofacitinib 10 mg b.i.d. will be approved on both sides of the pond for ulcerative colitis. It is probably a mistake to assume that the complete response letter to Pfizer regarding tofacitinib for psoriasis portends a negative judgment on the TOFA ulcerative colitis registration by either FDA or EMA.


  • About 25% of vedolizumab scrips are being written for anti-TNF naive patients. The response time is very long vs anti-TNF therapy, so the major drivers for choosing vedolizumab before anti-TNF are 1) patient’s disease burden – lower supports vedo use upfront), 2) patient’s infection risk, 3) patient’s aversion to biologics that increase infection risk and 4) cost (in Europe, vedolizumab is much less expensive than branded anti-TNF therapy)


  • Etrolizumab’s efficacy looks to be very similar to vedolizumab, in both ulcerative colitis, and the less well-studied Crohn’s population. The key product differentiation will be the dose form: vedolizumab is delivered as a 30 minute weight independent iv infusion. Etrolizumab is an injectable product. This Panel tends to see infusion as the better way to go, particularly in the Crohn’s population. However, vedo is a fixed dose, as opposed to e.g. infliximab which is weight based, and Panelists think the fixed dose limits their optimizing of a vedolizumab-based strategy.


  • Biosimilar anti-TNF is non-inferior to the parent brand when used in anti-TNF naive patients, but is inferior when switching due to antibody cross reactivity. Strategies to price the biosimilars at 20% below brand are being met by price matching by the innovator.


  • S1P agonists are more likely to have a long term therapeutic benefit than is mongersen.


  • NK cell inhibition is probably associated with better outcomes in IBD than is NK cell sparing.


Ulcerative Colitis / Crohn’s

Thought Leader Panel #20 2015-11

Therapeutic Area: Inflammatory Bowel Disease

Disease Area(s): Crohn’s disease, Ulcerative Colitis

Specialty/Location: Gastroenterology / N. America, Europe

Publication Date: November 2015

Principal Authors: Tricia L. Hanlon; Jeff Berk

If you are pharma, please contact Jeff Berk jeff@boltinternational.com for pricing for this report.

If you are a patient, please have your physician contact us for a free copy of this report.  We do not distribute directly to patients.


Product Code: Gastro-20-2015-11




(August 26 2014)

Reducing immunosuppression without allowing tumor regrowth, i.e. trying to prevent GVHD without abrogating the graft vs leukemia effect, is the Holy Grail of transplant biology.   Like the Grail, really effective ways of achieving this goal haven’t been demonstrated in completed randomized trials.  But there are, finally, plausible hypotheses to explain the underlying pathophysiology of graft vs host disease, and there are therapeutic approaches in the clinic that may capitalize on this new understanding.


The three problems after transplant that patients with malignant disease face are that they may have GVHD, their cancer may relapse, and they may have a fatal infectious complication.  On the one hand, patients with six log reduction of AML, CML, CLL or myeloma are exceedingly unlikely to relapse, and physicians can be more focused on immunosuppression to reduce GVHD.  Aggressive preventive therapy is limited mainly by the risk of increased infection.  On the other hand, if the patient is progressing with their cancer it is generally a losing proposition to immunosuppress them, and the treater finds his options to be extremely limited.  Net, monitoring the disease while trying to focus on the immunity constitution and avoiding GVHD is analogous to balancing on a three legged stool.  You can’t win transplant without doing all three of those things.  Setting aside the technical complexity of the operation, the solid organ transplanter, who doesn’t have to consider cancer relapse, has a relatively easier long term task.


BOLT / MedPredict’s Hem/Onc Thought Leader Panel (TLP) #39 summarizes the perspectives of six renowned US and European Thought Leaders who specialize in the treatment of graft-vs-host disease.  The Ad Board was run in August 2014.  This report updates the findings of a similar Ad Board conducted in the Summer of 2013.  For tracking purposes, TL comments from the current Ad Board are in BLUE font, while those from the 2013 Ad Board are in GREEN font.


This report is 193 pages in length.  It is organized by indication (acute, chronic, prevention, treatment), and then the mechanisms of action and drugs are grouped by their intended point of impact on GvHD pathophysiology: inflammation, lymphocyte trafficking, T-cell dysregulation, and end organ repair.





The Panel discussed the following topics / drugs:


GVHD – The big picture

Market Size (US, Annual)


Chronic GVHD

Acute GVHD

GVHD Risk Factors


Prevention of GVHD in Allogeneic Transplant Patients

Myeloablative vs Non-Myeloablative Transplants

Chronic GVHD Prevention Trials

Acute GVHD Prevention Trials


Acute GVHD Treatment

Treatment of Acute GVHD (Steroid Responsive)

Protocols for Steroid-Responsive or Steroid-Incomplete Responder GVHD

Treatment of Acute GVHD (Steroid Refractory)



Chronic GVHD Treatment

Treatment Flowchart cGvHD

Treatment of cGvHD according to organs involved

Chronic GVHD Treatment Trials




Pentostatin   deoxycoformycin


Actemra RoActemra tocilizumab  Roche


BEGEDINA® (Adienne)


Lymphocyte Trafficking

Anti-adhesion molecules Integrins, 47

vedolizumab / natalizumab / MadCAM


Adcetris brentuximab


maraviroc (Selzentry) Pfizer


Dysregulated Immunity / Delayed Generation of T-Regs

Low Dose IL2 (Dana Farber)

high dose cyclophosphamide

Extracorporeal photopheresis

Epigenetics:  Hypomethylating Agents / HDACs


Zolinza (vorinostat; Merck)


CliniMACS (CD34 selection; Miltenyi Biotec)

Proteasome Inhibition

Velcade (bortezomib; Takeda)

JAK (could have been filed under Lymphocyte Trafficking)

Jakafi Jakavi ruxolitinib

fostamatinib  Rigel


Campath alemtuzumab  + TBI +  temsirolimus

Regenerex, Novartis


ATG-Fresenius S: Neovii Biotech Fresenius

Gene Modified Donor T-Cells

Suicide Genes

BPX-501; Bellicum

TK008 (Molmed)

B-Cell  CD20   CD19   BTK

Rituxan / MabThera; rituximab (Roche)

obinutuzumab GA-101

ibrutinib (Pharmacyclics / Janssen)

CD19 CARS (Chimeric Antigen Receptor)

IL17 / IL23 / TH1 / TH17


End Organ Repair

Mesenchymal Stem Cells

Prochymal; remestemcel-L (Osiris)

MultiStem (Athersys / Pfizer)


F652  Generon (Shanghai China)






Latest News (May 7 2014)

Cancer Immunotherapy; Melanoma, Non-Small Cell Lung Cancer, Renal Cell Carcinoma is the 38th hematology/oncology Thought Leader Panel published by BOLT International.  We conducted in-depth interviews with ten peer recognized experts in the treatment of these three diseases.  We asked them to summarize the successes and challenges in establishing immunotherapy as a co-pillar of modern cancer treatment along with chemotherapy and targeted therapy.  And while other solid tumors can already be added to the list, the thought leaders focused on these three as they evaluated checkpoint inhibitors (certainly too narrow of a description), tumor infiltrating lymphocytes, biological response modifiers, vaccines and chimeric antigen receptors.  This report captures their collective wisdom.

As with all of our reports, we (reasonably) expect that Pharma foots the bill, but if you are a patient with one of these diseases, we will gladly share WITH YOUR PHYSICIAN (he must directly contact us and ask) relevant excerpts.



Keywords in this report: checkpoint, ipilimumab, Yervoy, MK-3475, Merck, nivolumab, BMS-936558 , Bristol-Myers Squibb, BMS, BRAF, MEK, Pegasys, interferon, aldesleukin, Prometheus, Avastin, bevacizumab, sunitinib, Votrient, pazopanib, GlaxoSmithKline, Inlyta, axitinib, Afinitor, everolimus, Novartis, MPDL3280A, Roche, Genentech, tremelimumab, AstraZeneca, MedImmune, MSB0010718C, EMD Serono, MEDI0680, MEDI4736, BiocerOX, pidilizumab, CT-011, CureTech, Teva, ANB011, AnaptysBio, OX40, Medimmune, BMS663513, urelumab, 41-BB, CD137, PF-05082566, PF-2566, Pfizer, TRX-518, GITR, VISTA, B7-H5, Gi24, Dies1, Janssen, ImmuNext, B7-H3, CD276, MGA-271, Servier, Macrogenics, LAG-3, lymphocyte-activation gene 3, CD223, BMS-986016, IMP321, IMP701, Immutep, TIM-3,T cell immunoglobulin and mucin domain 3, Brigham & Women’s, IDO, Indoleamine 2, 3-dioxygenase, INCB24360, Incyte, indoximod, NewLink, NLG919, NewLink, KIR, lirilumab, MICA, IPH4102, Innate Pharma, PS, phosphatidyl serine, bavituximab, Peregrine, TIL, tumor Infiltrating lymphocytes, adoptive T-cell transfer, biological response modifiers, IL-2, Pegasys, Roche, Proleukin, High Dose IL2, Prometheus, IL12, Ad-RTS-hIL-12, Ziopharm, T-cell Vaccines, talimogene laherparepvec, T-VEC,  Amgen, AGS-003, Argos, Tumor Associated Peptide Vaccines, IMA901, Immatics Biotechnologies GmbH, CAR, Carbonic Anhydrase IX CAR, Kite Pharmaceuticals, Anti-VEGFR2 CAR,  NIH, melanoma, non-small cell lung cancer, renal cell carcinoma, PD-1, PD-L1, CD274, B7-H1, PD-L2, CD273, B7-DC, PD-L4, CTLA4, B7.1, CD80, B7.2, CD86, repulsive guidance molecule b, RGMb




Latest News (December 4 2013):

In BOLT / MedPredict’s Psoriasis Thought Leader Panel #25 2013-12, seven of our experts (6 derms, 1 rheum; 4 US, 4 EU) in the treatment of moderate/severe psoriasis and moderate/severe psoriatic arthritis share their year-end views on the strengths and weaknesses of key competitors in development for these indications.


Psoriasis often appears between the ages of 15 and 25, but can develop at any age.  Psoriatic arthritis usually develops between the ages of 30 and 50.  Coupling these age of onset statistics with the experience that patients cycle through antipsoriatic therapy on average each 18-24 months, one realizes that there will be room for many new competitors in this space.


However, most of our thought leaders say that they will try two therapies from a class before moving on to a new mechanism of action.  This tempers the commercial opportunity for the 3rd, 4th and 5th competitor unless there is a significant benefit to the patient, physician or payer.


For the patient, there is a new paradigm: reaching PASI 100 is an attainable goal for more than 50% of patients with moderate / severe psoriasis (see IL17 inhibitors).  For the physician, “methotrexate without monitoring” offers a safe, easy to manage therapy (apremilast) for more moderate cases.  For payers, biosimilar versions of etanercept (in the EU) and adalimumab (worldwide) are imminent.


Against this backdrop our Panel talks about the most recent trial data for the following mechanisms of action and molecules:


TNF: adalimumab, etanercept, golimumab, certolizumab, ABP-501, PF-06410293, CT-P13, CHS-0214

IL23: ustekinumab, tildrakizumab, guselkumab, BI-655066

IL17: brodalumab, secukinumab, ixekizumab

IL17 / TNF: ABT-122


JAK: tofacitinib, baricitinib, GSK2586184, INCB039110, ASP015k, PF-04965842, ABT494

PDE4: apremilast

IL6: clazakizumab

Fumarate: XP-23829, LAS-41008

Innate Immunity


(September 22, 2013):

Non-Small Cell Lung Cancer

BOLT / MedPredict NSCLC Thought Leader Panel #36, published September 2013, shares key insights gleaned from our Panel of experts in non-small cell lung cancer during interviews we conducted since ASCO 2013.  This report focuses on adenocarcinomas and squamous cell carcinomas of the lung.  There is little discussion of other lung cancers with partial or IHC adenocarcinoma differentiation (e.g. large cell carcinomas, small cell carcinomas or large cell endocrine carcinomas, brief comments on adenosquamous carcinomas in the section on the SQUIRE trial with necitumumab).  The report is generally organized by target mechanism.

More than a decade since EGFR was identified as a substantial driver for adenocarcinomas, and five years since the importance of ALK fusions was shown, the targets for treatment of this histology has matured.  We share our Panel’s opinions on next generation EGFR and ALK inhibitors, and newer targets: ROS, RET, HER2 and others.

In contrast, squamous cell carcinomas of the lung lack an approved targeted therapy.  While less mature, it looks like this will change shortly, as FGF1 inhibitors make their way through development.

The major story in the solid tumor world this year has been the explosive development in the area of checkpoint modulation. There is speculation that PD-1 and other checkpoint approaches will be most beneficial in the squamous NSCLCs.  The Panel reviews the safety and efficacy data presented on the PD-1 and PD-L1 inhibitors.

Finally, the Panel sheds light on PI3K in brain metastases, CDK4/6, HSP90 and other topics that will impact the changing landscape of NSCLC in the next few years.

Mechanisms / Drugs discussed in this report:

ALK, Xalkori, crizotinib, Pfizer, LDK378, Novartis, AP26113, Ariad, RO5424802, CH5424802, AF802, Chugai, Roche, ASP3026, Astellas,

AXL, BGB324, BerGenBio,

CDK4/6, LY2835219, Lilly,

CTLA4, Yervoy, ipilimumab, BMS,

DDR2, Sprycel, dasatinib, BMS,

EGFR, Tarceva, erlotinib,  Genentech, Astellas, necitumumab Lilly, CO-1686, Clovis, AP26113, Ariad, AZD9291, AstraZeneca,

EGFR/HER2, Gilotrif, afatinib, Boehringer-Ingelheim, dacomitinib, Pfizer,

FGF, BGJ398, Novartis, JNJ-42756493, Astex, Janssen, AZD-4547, AstraZeneca, Iclusig, ponatinib, Ariad, LY-2874455, Lilly, SSR128129E, Sanofi-Aventis,

Folate, Alimta, pemetrexed, Lilly, vintafolide, Merck, Endocyte,

HSP90, ganetespib, Synta, AUY922, Novartis, AT13387, Astex, retaspimycin, IPI-504, Infinity,


MEK, selumetinib, AstraZeneca, Array, MEK-162, Novartis, Array,

MET, onartuzumab, MetMAb, Genentech,

MUC1, Stimuvax, L-BLP25, Oncothyreon, Merck Serono,

PD-1, PD-L1, MPDL3280A, Genentech, lambrolizumab, MK-3475, Merck, nivolumab, BMS, Ono, ANB011, AnaptysBio,

PI3K, brain metastases,

PS, bavituximab, Peregrine,

Reovirus, Reolysin, pelareorep, Oncolytics,

RET Fusion, cabozantinib, Cometriq, Exelixis, Iclusig, ponatinib, Ariad,

ROS1, Xalkori, crizotinib, Pfizer,

Vaccine, MAGE-A3, GlaxoSmithKline, Agenus,

VEGF, Avastin, bevacizumab, Genentech, Vargatef, nintedanib, Boehringer-Ingelheim






Latest News (July, 2013):

We’re Closing Our Doors

Since BOLT’s first day of business in 1996, and MedPredict’s in 2006 we have been reachable to help our clients.  Last July 4th one of our clients tracked me down in Northern Idaho (yes, they have cell phone service.  Sort of) for an emergency project.  But this year, come the end of July, some of us are going to Sierra Prieta (google it) to dig latrines and not shower for a week.  We have this expression in our office: “That’s a 1st World problem”.  Even as we work to help patients receive and Pharma develop new therapies for hard to treat diseases, we are working on 1st World problems.  But “I have to carry water two miles this morning”, well, that’s definitely a 3rd World problem.  And we want to get out of the office, out of Snottsdale AZ, and live for a week like most people on Earth do.  It’s one thing to talk about solving the world’s problems; and sending money is pretty much just talk.  It’s another to go lay pipe.  So we’re going to dig ditches and lay pipe.  See you when we’re back and showered.

– jb





Looking to access BOLT’s Syndicated Thought Leader Panel reports? Over the past 15 years BOLT International has moderated over 4,000 Thought Leader interviews across a wide range of therapeutic categories.  These are summarized and analyzed in BOLT’s Thought Leader Panels; many of which are available to the public.  Contact me by email to discuss pricing (jeff@boltinternational.com).  We have recently installed a “buy now” feature on this website.  There you will see our most current releases, available for instant purchase by credit card.  If you don’t see what you want, ask.  A note to patients:  we discount our pricing (sometimes down to $0) to bona fide patients on a case-by-case basis – especially if our information will help you and your physician improve your care.  Seriously, we’ll need a note from your doctor!

Competence – BOLT International’s core competence is the integration of healthcare and pharmaceutical information sets into insightful commercial strategies. Our comprehensive understanding of healthcare product lifecycles – from biotech start-ups through research and clinical development, and onto global marketing, pricing and reimbursement strategies – permits us to develop concise, actionable recommendations.

Experience – BOLT’s leadership position in Healthcare Competitive Intelligence is derived from years of professional experience in both the science and the business of healthcare. BOLT’s principals know the industry, the firms, the markets, the politics and the technologies. This experience base – enhanced with BOLT’s THOUGHT LEADER physician panels, and our secondary information gathering and analysis techniques – permits us to provide actionable recommendations to a wide-variety of healthcare industry clients.

Knowledge – BOLT’s THOUGHT LEADER panels give us proprietary access to decision makers (physicians, patients, payers and regulators) in numerous geographies. This in turn drives our understanding of key issues and development of winning strategies – Strategies that reflect a complete analysis of the events predictive of both the direction and the rate of change within the healthcare industry. As a result, you’ll implement sound decisions with the confidence that your actions are based on the most comprehensive competitive, technical and financial analyses available.

Attention – BOLT provides the attention to service and detail that can be missing when dealing with large, general competitive intelligence firms. Our ability to meet your timing needs and to deliver the quality of analysis you demand is unparalleled.