New expansion bone team

Sorry to say, but if you were flown to San Fran and have not heard yet, an offer was made to another candidate.

 

The division will be gone in a year anyway

 

I assumed that too. I was disappointed that a courtesy call or even an email was not given.

 

They probably want to see if the cabdidates pass the background test and drug screen before officially closing out all candidates don't you think?

 

Not a chance in hell-probably safest division at Amgen-
CV- too many Repatha reps- poor outcomes data
OBU- too many reps not enough revenue
INBU-too many reps and an old drug
BCBU-too many reps-poor Repatha outcomes data

Bone team- not the many reps, nice niche product
those are the facts

 

to be a "safe" division, you must pay for yourself....good luck with that...how many Romo patients? How much will it have to cost to pay for the division overhead?...do the math, and then see how safe you feel.

 

math is better in the Romo division than any other-sorry you stayed where you are--layoffs are coming soon and the Romo division is the only division that will not be touched--have fun looking for a new job

 

smallest sales force dopey--will become profitable just like Forteo was--have fun selling Repatha--the worst biologic to sell in the history of biologics

 

Let me help you out with the math and the value of each patient


1000 Repatha patients X $14,400 X 10 Years = 140,000,000

2000 Repatha patients X $14,4000 X 10 Years = 280,000,000

1000 Romo patients X $20,000 X 1 year = $20,000,000

2000 Romo Patients X $40,000 X 1 year = $80,000,000

So, What exactly is the indication? How many ROMO patients are there? How much will it cost? and what does your sales force cost per month? How much of that pie is left over after Generic Forteo, & Abalaparatide, which both have superior data. These are the questions that many reps and DM's understood and decided to stay with their current team.

 

Hahahahahahaha!!! See how big pharma Amgen has become!!! Romo is Part B-less side effects, with great efficacy-check out BMD, less dosing. With 8-10 reps selling Repatha covering the same area as one Romo rep. Romo reps have similar geographies that most reps who sell biologics outside of the PCSK9 nightmare. Go back to Daiichi, Astrazenca or Merck.

 

more like 10-12 repatha reps-get your numbers straight!

 

Romo is not going to get approved. Negative FDA meeting predict problems. -SB

 

The whispers have been around for about a month

 

i call BS on this one-what is the reason for this not to be approved??

 

Binding antibodies were seen in 20% of the romosozumab group, and antibodies with in vitro neutralizing activity in 3%. In contrast, no binding antibodies were seen in any of the other treatment groups. However, the development of antibodies appeared to have no effect on adverse events, pharmacokinetics, or pharmacodynamics, the investigators note.

This is why, FDA wants more data on the long term effect with the Binding anibodies issue.

 

Upon other things.....use your google skills....dig around in sclerostin inhibition....what's one of your major call points? That's it, no more hints.

 

Typical amgen long term rep - just drink the koolaid and is too lazy and dumb to think for himself. Open your eyes and do your own research dumbass. This is why the best reps never stay at Amgen. They know what's up. They also know more about the product than what you get at training. This initiative is why oth r companies want them now checking the box pcp sampler dropper that you are

 

We're screwed, why the hell hire all these people!! Repatha better get the outcomes data this summer or there will be a massive layoff next fall.

 

It all really depends on how impressive managed care views the new data. Once in label, unless it's like DAMN that's good, they won't be loosening restriction for another year or two. Amgen wants to go back and renegotiate but that chip depends on how good the data is and what price MCO think it justifies. If Amgen sticks to it's high price guns and isn't convincing, expect crappy access still. The longer the access sucks, the more damage will be done in your doctors eyes. Even if access improves in 3-4 years, that's a slow launch and your doctors will need convincing that the drug is worth their effort. It's like convincing an ex-GF you've cheated on 3-4 times that you won't do it again. Aka it's an uphill battle unless the data is phenomenal. If it's mediocre, then access will depend on how much amgen is willing to drop the price per the value mco believe the drug to be. I think amgen will be cocky and expect more access issues.

 

Advertisement

.

View Full Text

A surprising role for sclerostin in arthritis
Antibodies that block the activity of sclerostin, a bone destruction molecule, are in clinical trials for the treatment of osteoporosis. But these antibodies may not be safe for certain patients: those with inflammatory rheumatoid arthritis (RA). Wehmeyer et al. were surprised to find that sclerostin inhibition did not stop bone loss and actually aggravated disease in an animal model of RA that was dependent on tumor necrosis factor α (TNFα); two other rodent RA models with minimal or no dependence on this inflammatory cytokine were unaffected. The authors found that sclerostin blocks TNFα-induced p38 and NFκB activation—key steps in RA development. Thus, sclerostin appears to have a protective role in TNF-mediated chronic inflammation, and inhibiting it would be contraindicated in a subset of RA patients. This study therefore has immediate implications for current clinical trials involving patients with inflammatory bone loss.

Abstract
Sclerostin, an inhibitor of the Wnt/β-catenin pathway, has anti-anabolic effects on bone formation by negatively regulating osteoblast differentiation. Mutations in the human sclerostin gene (SOST) lead to sclerosteosis with progressive skeletal overgrowth, whereas sclerostin-deficient (Sost−/−) mice exhibit increased bone mass and strength. Therefore, antibody-mediated inhibition of sclerostin is currently being clinically evaluated for the treatment of postmenopausal osteoporosis in humans. We report that in chronic TNFα (tumor necrosis factor α)–dependent arthritis, fibroblast-like synoviocytes constitute a major source of sclerostin and that either the lack of sclerostin or its antibody-mediated inhibition leads to an acceleration of rheumatoid arthritis (RA)–like disease in human TNFα transgenic (hTNFtg) mice with enhanced pannus formation and joint destruction. Inhibition of sclerostin also failed to improve clinical signs and joint destruction in the partially TNFα-dependent glucose-6-phosphate isomerase–induced arthritis mouse model, but ameliorated disease severity in K/BxN serum transfer–induced arthritis mouse model, which is independent of TNF receptor signaling, thus suggesting a specific role for sclerostin in TNFα signaling. Sclerostin effectively blocked TNFα- but not interleukin-1–induced activation of p38, a key step in arthritis development, pointing to a previously unrealized protective role of sclerostin in TNF-mediated chronic inflammation. The possibility of anti-sclerostin antibody treatment worsening clinical RA outcome under chronic TNFα-dependent inflammatory conditions in mice means that caution should be taken both when considering such treatment for inflammatory bone loss in RA and when using anti-sclerostin antibodies in patients with TNFα-dependent comorbidities