HGH Suppression Timing Debate/ Calling All Experts

[dans]

After reading several threads from different boards including this one there seems to be a debate over GH injection timing. This debate stems from lack of knowledge of EXACTLY how long Injected HGH suppresses Natural HGH.

It is a known fact that GH injection will suppress natural HGH production to some degree. The debate seems to hinge on how long this suppression lasts.

Some people are claiming that it will suppress your natural GH for 4-6 hours.

Most of the research that recommends bedtime injections is aimed at the individual with a non-functioning pituitary. Children with severe growth disorders and those adults who have lost pituitary function from illness, radiation treatments, AIDS, or accidents should dose GH at bedtime so as to mimmick the natural rythyms of the healthy human endocrine system.
But those who are HRT patients and bodybuilders should not. Why? Because we retain normal GH secretions, although perhaps somewhat diminished in the older lifter. ExoGH only makes the pituitary a little "lazy" for a few hours.....it is not shut down like in testosterone supplementation. Since we produce up to 80% of our natural GH during the first 2 hours of deep sleep, why not take advantage of that and dose our exoGH at a flat time like late afternoon?
Even Genentech makes this distinction now in the instructions to physicians. They specify non-bedtime injections for HRT, bedtime for sick people. Genentech invented synthetic somatropin and holds the first FDA approval for medical use.

Others have claimed it will suppress your natural GH anywhere from 12-24 hours.

ok.. time to throw a monkey in the wrench.. here is an article found (courtesy of Nandi)...
http://jcem.endojournals.org/cgi/co...ll/85/2/601#R31

"The reduction of serum 22K-hGH level after 20K-hGH administration required a period of ca. 4 h, and the level tended to recover by 24 h. However, the delay in suppression of endogenous 22K-hGH by exogenous 20K-hGH is difficult to define precisely because of the intermittent nature of hGH secretion"


basically once exogenous gh is administered, endogenous is suppressed for about 24hours.. Plus we forgot to take into consideration that IGF-1 also suppresses natural gh, so now we have (2) components working together to suppress endogenous... which therefore will keep natural gh suppressed for ~24hours...

so.. bedtime shots which is what i have testified to all along seem to be the best to do... you shoot your gh, go to sleep, get your natural peak, then the exogenous gh kicks in (takes ~4 hrs to kick in) and then gh is active for quite some time... so this way you get almost double the dosage Natural and exog in one night!!!

Others have claimed it will not start suppressing your natural GH until 4-6 hours after you inject and then continue for 12-16 hours.

The researchers considered the impact of exogenous GH on endogenous 22K-hGH secretion during the first 6 hours after GH administration insignificant:

..."There were no significant changes in the AUC0–6 h between the 20K-hGH-treated and placebo groups..."

The greatest suppression was noticed from 6-12 hours after administration.

From 12-18 hours & 18-24 hours endogenous GH "tended to be suppressed in the 20K-hGH-treated groups, although differences were not significant compared with the placebo group."


So you still have to worry about IGF-1 negative feedback loop although GH levels would drop.....

"On the other hand, serum IGF-I levels were not increased significantly at 4 h, but were increased at 8, 12, 24 , and 36 h"

NOTE: NONE OF THE THREE PREVIOUS QUOTES ARE MY OWN, THEY ARE TAKEN FROM THIS THREAD(A VERY INTERESTING READ):http://www.steroidology.com/forum/sh...?threadid=4157

This post courtesy of RedBaron seems to answer some questions but still no definitive answers, and it conflicts with a couple of the earlier quotes from the other thread:

The problem we will always have with subjects such as this is that everyone's body runs just a little different. As JohnnyB mentioned, it is pretty difficult to time with precision when the liver is going to secrete IGF-1. That being the case, unless we have some definitive monitoring device to verify the timing of that release, it is going to be even more difficult to time our HGH injections using this as a criteria.

There is no question that waking up at 3-4 a.m. and giving yourself an injection has a lot of merit. I did this for about 10 months while I was using Genotropin Mini-Quick .8mg HGH. No question about it working well. The next best time to inject is first thing in the morning before you ever get dressed. These two times are going to offer the least chance of disrupting your own HGH cycle .... but as I said, everyone runs a little different so we are really making some general observations.

Realize that there are about 8-10 pulses of HGH throughout the day ... not ONLY the one at night. The thing is the chemical and hormonal conditions of the body at night are conducive to a major release of HGH. Other times you will see a MAJOR release of HGH is during short duration, HIGH intensity working out. If you have ever experienced a REALLY intense leg day workout the nauseous feeling and tiredness that follows is many times the result of a big endogenous HGH dump into your system. HGH is going to work for you for the most part whenever it is released into you system.

The reasoning behind a night-time injection would make a LOT of sense for someone with low / no natural HGH. This would most closely mimic the body's own cycle. For those of us with a normal / high natural output, night-time injections are a bit more complex issue. The thought behind the normal early morning - early afternoon injections is because these are times when your body's cortisol levels are high, and HGH can assist in minimizing its potential for catabolism. Also these are times that offer a greater likelihood of not interfering with a great number of natural pulses of endogenous HGH (though certainly no guarantee because of some of the variables discussed here).

So ..... I think about as close as anyone could come to a consensus would be to say .... If you are the type of person that routinely gets up to go to the bathroom in the early morning hours, that is a PERFECT time to take an HGH injection. If you aren't, next best is going to be the second you wake up. If you are taking two injections per day, there are a few scenarios that would make sense, such as (roughly most desirable to lesser):

injection one at 2-3 a.m. at bathroom break, number two at 8-9 a.m. upon waking
injection one at 2-3 a.m. at bathroom break, number two at 1-2 p.m.
injection one at 7-9 a.m., number two at 1-2 p.m.

If your natural HGH production is non-existant -
injection one at bedtime, injection two first thing upon waking
injection one at bedtime, injection two 1-2 p.m.

So what is the answer to this question?

Is there one yet, or are there not enough studies?

Hopefully someone has some answers, or at least we can get some more serious discussion going regarding this issue.

[DieselNYC80]

Bump this

Ive been wondering if anyone really has an answer to this.....

[Pinnacle]

Here's one post I happen to like,and agree with.My doc agreed to this post as well.I printed and showed him this..

Originally Posted by Slic4788
Found this earlier...it might help.

Credit goes to Einstein(former member):

GH is regulated in a pulsatile manner. It's released from the pituitary in response to GHRH from the hypothalamus....once GH is released, it carries out its actions, one of which is causing increased expression of IGF-1, primarily in the liver. it's IGF-1 that's the main negative feedback inhibitor of further GH release.....as long as there is sufficient serum IGF-1 levels, somatostatin is expressed, which prevents GHRH from causing further release of GH. Normal GH pulses occur about every 4-5 hrs, so taking exo GH (or LR3) will suppress 1-2 pulses if taking GH, 2-4 if using LR3. Once these compound are at low enough levels again, somatostatin expression is reduced and GHRH predominates and causes further GH release from the pituitary, and the normal pulse pattern resumes.........

There really is no recovery period from GH, because you're never fully suppressing the HP axis regarding GH....you're only doing so for part of the day, unless you're doing very high doses of GH or dosing E4hrs or so. Using LR3 >1x/day can also cause suppression for a full day, but even then, i don't think there would be any long term problems.


But Rodge had this to say about HGH suppression..

my last blood work i did was 3 days after my last hgh shot.the test came back and my igf-1 levels were 453 ng/ml.
i would call that still elevated and thus supresive.

-rodge

~Pinnacle~

[Mr. Sparkle]

I bet GHRP would help prevent any GH suppresion....

[Pinnacle]

I bet GHRP would help prevent any GH suppresion....

How so Mr Sparkles?I'm curious as to your theory.Explain if you will.


~Pinnacle~

[alo5603]

yeah there is a lot of different opinions on it, and it is really hard to follow which one. I have been in this boat ever since i tried GH. Do what you think is right but allow other GOOD opinions help in your decision.

alo

[Mr. Sparkle]

How so Mr Sparkles?I'm curious as to your theory.Explain if you will.


~Pinnacle~

couldnt you just take a little twice ED and maintain your natty GH level?

[Pinnacle]

couldnt you just take a little twice ED and maintain your natty GH level?

As far as HGH dosing?I believe you can.AM dose followed by an early afternoon dose.That's my protocol anyway.


~Pinnacle~

[dans]

That logic seems sound but it all depends on the timing of the suppression of your natural levels. If the suppression does not start for 6 hours and then continues for 12 hours a nightime injection would make more sense.

I was hoping someone would have some hard scientific facts about exactly how the suppression of your natural levels works. Right now it seems to be a gray area, some people claiming one thing, others claiming something else.

If there were some definitive answers on the timing of the suppression then it would be easy to figure out the best times to inject. Right now there seems to be a difference of opinion on how long and how much natural GH levels are suppressed after an injection.

I would like to get to the bottom of this, but it may take a doctor or someone with extensive knowledge to explain this.

Maybe there is not an answer right now, because of lack of studies, but hopefully that is not the case.

[dans]

Bumping this......

[Pinnacle]

Possibly your answer might,just might be in one of these links.

Check this out..

http://forums.steroid.com/showthread.php?t=197366

~Pinnacle~

[dans]

Thanks Pinnacle, that thread has plenty of places for me to search for studies. I will post if I find anything useful regarding this subject.

[dans]

Found something very informative already:

Recovery of Growth Hormone Release from Suppression by Exogenous Insulin-Like Growth Factor I (IGF-I): Evidence for a Suppressive Action of Free Rather Than Bound IGF-I1
Ian M. Chapman2, Mark L. Hartman, Karen S. Pieper, Emily H. Skiles, Suzan S. Pezzoli, Raymond L. Hintz and Michael O. Thorner

Division of Endocrinology and Metabolism, Department of Medicine (I.M.C., M.L.H., E.H.S., S.S.P., M.O.T.), and Division of Biostatistics and Epidemiology, Department of Health Evaluation Sciences (K.S.P.), University of Virginia Health Sciences Center, Charlottesville, Virginia 22908; and the Department of Pediatrics, Stanford University Medical Center (R.L.H.), Stanford, California 94305

Address all correspondence and requests for reprints to: Dr. Michael O. Thorner, Department of Medicine, Box 466, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908.

To determine the time course of recovery of GH release from insulin-like growth factor I (IGF-I) suppression, 11 healthy adults (18–29 yr) received, in randomized order, 4-h iv infusions of recombinant human IGF-I (rhIGF-I; 3 µg/kg·h) or saline (control) from 25.5–29.5 h of a 47.5-h fast. Serum GH was maximally suppressed within 2 h and remained suppressed for 2 h after the rhIGF-I infusion; during this 4-h period, GH concentrations were approximately 25% of control day levels [median (interquartile range), 1.2 (0.4–4.0) vs. 4.8 (2.8–7.9) µg/L; P < 0.05]. A rebound increase in GH concentrations occurred 5–7 h after the end of rhIGF-I infusion [7.6 (4.6–11.7) vs. 4.3 (2.5–6.0) µg/L; P < 0.05]. Thereafter, serum GH concentrations were similar on both days. Total IGF-I concentrations peaked at the end of the rhIGF-I infusion (432 ± 43 vs. 263 ± 44 µg/L; P < 0.0001) and remained elevated 18 h after the rhIGF-I infusion (360 ± 36 vs. 202 ± 23 µg/L; P = 0.001). Free IGF-I concentrations were approximately 140% above control day values at the end of the infusion (2.1 ± 0.4 vs. 0.88 ± 0.3 µg/L; P = 0.001), but declined to baseline within 2 h after the infusion. The close temporal association between the resolution of GH suppression and the fall of free IGF-I concentrations, and the lack of any association with total IGF-I concentrations suggest that unbound (free), not protein-bound, IGF-I is the major IGF-I component responsible for this suppression. The rebound increase in GH concentrations after the end of rhIGF-I infusion is consistent with cessation of an inhibitory effect of free IGF-I on GH release.

According to this study, your total IGF-I number may not be an indicator of GH suppression. Only the FREE IGF-1 is responsible for GH suppression.

More about GH suppression:

Changes in Free Rather Than Total Insulin-Like Growth Factor-I Enhance Insulin Sensitivity and Suppress Endogenous Peak Growth Hormone (GH) Release following Short-Term Low-Dose GH Administration in Young Healthy Adults
Kevin Yuen, Jan Frystyk, Margot Umpleby, Linda Fryklund and David Dunger

Department of Paediatrics (K.Y., D.D.), University of Cambridge, Cambridge CB2 2QQ, United Kingdom; Medical Research Laboratories (J.F.), Aarhus University Hospital, Aarhus, Denmark DK-8000; Department of Diabetes and Endocrinology (M.U.), Guy’s King’s and St. Thomas’ School of Medicine, King’s College, London SE1 7EH, United Kingdom; and Pfizer Health AB (L.F.), Stockholm SE-11287, Sweden

Address all correspondence and requests for reprints to: Professor David B. Dunger, University Department of Paediatrics, Level 8, Box 116, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom. E-mail: [email protected].

High-dose GH administration is commonly associated with impaired insulin sensitivity (SI) in humans. Paradoxically we have shown that low-dose GH (1.7 µg/kg·d) administration enhances ß-cell function in young healthy adults. In the present double-blind, placebo-controlled, cross-over study, we explored the physiological effects of this low GH dose on glucose metabolism in 12 young healthy adults (seven males, 19–29 yr). At pretreatment and after each 14-d treatment block, overnight metabolic profiles were assessed followed by a hyperinsulinemic euglycemic clamp, whereas fasting blood samples were collected weekly.

In subjects treated with GH first (group A, n = 6), GH treatment increased total IGF-I (P < 0.05) and IGF binding protein-3 (P < 0.01) after 7 d, but these levels subsequently returned to pretreatment levels after 14 d. In contrast, free IGF-I increased (P < 0.05), and overnight GH pulse peak amplitude decreased (P < 0.01) after 14 d. In subjects treated with placebo first (group B, n = 6), all biochemical parameters were unchanged after placebo treatment, whereas the changes in free and total IGF-I were similar to those of group A after GH treatment. Combined clamp data from both groups A and B (n = 12) showed that 14-d GH treatment decreased overnight plasma insulin levels (P < 0.02) and hepatic glucose appearance (P < 0.05) and increased SI (P < 0.01). Of note, the GH-induced changes in SI positively correlated with the changes in free IGF-I (r = 0.72, P < 0.01).

In conclusion, low-dose GH administration enhanced SI and suppressed endogenous peak GH release, and we hypothesize that these effects are the direct result of increased serum levels of free IGF-I.

K.Y. is supported by a research grant from Pfizer Ltd., and J.F. is supported by a grant from the Danish Health Research Council.

Abbreviations: CV, Coefficient of variation; endoRa, glucose appearance; HOMA, homeostasis model assessment; IGFBP, IGF binding protein; NEFA, nonesterified fatty acid; Rd, glucose disappearance; SI, insulin sensitivity.

[Pinnacle]

So the first study suggests natural HGH output is suppressed for 5-7 hrs.If I'm reading that correctly.

~Pinnacle~

[dans]

So the first study suggests natural HGH output is suppressed for 5-7 hrs.If I'm reading that correctly.

~Pinnacle~

That is how I read it too Pinnacle.

Now check out this study, it may take awhile to wade through but carefully reading it is very interesting, especially the charts.

http://jcem.endojournals.org/cgi/content/full/85/2/601

This study was conducted on thirty-two 21-31 year old males. They administered the exogenous GH at 9PM and monitored HGH levels for the next 24 hours.

From reading the charts it looks like admnistering it at 9PM completely suppressed the natural release of HGH that was seen around 3AM by the placebo group, which would not be a good idea at all. In fact, it seems natural releases were pretty suppressed for the entire 24 hour period. This is how I am reading it.

This to me says 1 early morning injection would be best. Giving your body optimal time to fully recover for its big natural release in the middle of the next night.

What do you guys get from reading this study?

[dans]

Here is a study suggesting suppression of natural GH can last up to 4 days:

Changes in Non-22-Kilodalton (kDa) Isoforms of Growth Hormone (GH) after Administration of 22-kDa Recombinant Human GH in Trained Adult Males1
Jennifer D. Wallace, Ross C. Cuneo, Martin Bidlingmaier, Per Arne Lundberg, Lena Carlsson, Cesar Luiz Boguszewski, John Hay, Massoud Boroujerdi, Antonio Cittadini, Rolf Dall, Thord Rosén and Christian J. Strasburger

Metabolic Research Unit (J.D.W., R.C.C., J.H.), Department of Medicine, and Statistics Section, Department of Social and Preventative Medicine, University of Queensland, Princess Alexandra Hospital, Brisbane 4102, Australia; Neuroendocrine Unit (M.B., C.J.S.), Department of Medicine, Innenstadt University Hospital, 80336 Munich, Germany; Serviço do Endocrinologia e Metabologia do Hospital de Clínicas da Universidade Federal do Paraná (C.L.B.), 80060-240 Curitiba, Brasil; Research Centre for Endocrinology and Metabolism (P.A.L., L.C., T.R.), Sahlgrenska Hospital, Gothenberg, S-413 45 Sweden; Department of Endocrinology (M.B.), St. Thomas’s Hospital, London SE1 7EH, United Kingdom; Department of Internal Medicine and Cardiovascular Sciences (A.C.), Frederico II University, 80131 Naples, Italy; and Department of Medicine M (Endocrinology and Diabetes) (R.D.), Aarhus University Hospital, Aarhus, 8000 Denmark

Address all correspondence and requests for reprints to: Jennifer D. Wallace, Metabolic Research Unit, University of Queensland, Department of Medicine, Princess Alexandra Hospital, Brisbane 4102, Australia. E-mail: [email protected].

GH is being used by elite athletes to enhance sporting performance. To examine the hypothesis that exogenous 22-kDa recombinant human GH (rhGH) administration could be detected through suppression of non-22-kDa isoforms of GH, we studied seventeen aerobically trained males (age, 26.9 ± 1.5 yr) randomized to rhGH or placebo treatment (0.15 IU/kg/day for 1 week). Subjects were studied at rest and in response to exercise (cycle-ergometry at 65% of maximal work capacity for 20 min). Serum was assayed for total GH (Pharmacia IRMA and pituitary GH), 22-kDa GH (2 different 2-site monoclonal immunoassays), non-22-kDa GH (22-kDa GH-exclusion assay), 20-kDa GH, and immunofunctional GH. In the study, 3 h after the last dose of rhGH, total and 22-kDa GH concentrations were elevated, reflecting exogenous 22-kDa GH. Non-22-kDa and 20-kDa GH levels were suppressed. Regression of non-22-kDa or 20-kDa GH against total or 22-kDa GH produced clear separation of treatment groups. In identical exercise studies repeated between 24 and 96 h after cessation of treatment, the magnitude of the responses of all GH isoforms was suppressed (P < 0.01), but the relative proportions were similar to those before treatment. We conclude: 1) supraphysiological doses of rhGH in trained adult males suppressed exercise-stimulated endogenous circulating isoforms of GH for up to 4 days; 2) the clearest separation of treatment groups required the simultaneous presence of high exogenous 22-kDa GH and suppressed 20-kDa or non-22-kDa GH concentrations; and 3) these methods may prove useful in detecting rhGH abuse in athletes.

If this is true and you will be almost completely suppressing natural production if you are injecting HGH daily, why not do an injection at night to simulate your natural release?

[Pinnacle]

Quite interesting.All doctors that I know of recommend AM HGH shots.I'm sure you'll find more studies to back that up.I for one am not,nor ever was a believer in PM shots before bed.I believe in taking advantage of the natural release of HGH.I do however do an early afternoon shot as well as the AM shot.I think giving myself 12-13 hours before rem sleep occurs is ample time.But should you discover more studies that suggest otherwise,I'm more than willing to give the AM protocol a try.

~Pinnacle~

[alo5603]

Quite interesting.All doctors that I know of recommend AM HGH shots.I'm sure you'll find more studies to back that up.I for one am not,nor ever was a believer in PM shots before bed.I believe in taking advantage of the natural release of HGH.I do however do an early afternoon shot as well as the AM shot.I think giving myself 12-13 hours before rem sleep occurs is ample time.But should you discover more studies that suggest otherwise,I'm more than willing to give the AM protocol a try.

~Pinnacle~

I agree pinnacle, ive never done pm shots, just doesnt seem logical. There are others that do and claim good results, and i aint downin them, if it works for them, then they can keep doin it. Me, i will never do a pm shot.

alo

[Pinnacle]

Here is a study suggesting suppression of natural GH can last up to 4 days:





If this is true and you will be almost completely suppressing natural production if you are injecting HGH daily, why not do an injection at night to simulate your natural release?

That's rHGH though............

[dans]

Hey Pinnacle, if you have an hour or so to spare, take your time and completely read through that study I posted(http://jcem.endojournals.org/cgi/content/full/85/2/601) and let me know what you think. I have read it through once but I plan on studying it some more, I would like to know what someone else gets from it so we can discuss it further.

[dans]

That's rHGH though............

Your right Pinnacle, I misread that. But I am not sure I know the difference. I didn't know people were taking rHGH as well as HGH, or am I just reading that study completely wrong?

[dans]

That's rHGH though............

On further investigation, rHGH is what we are referring to as HGH:

The nomenclature for growth hormone is a bit complicated, but
understanding it from the beginning can save much confusion in the
future. Somatropin refers to growth hormone of the same amino acid
sequence as the naturally occurring growth hormone. Somatropin extracted
from the human pituitary gland was originally designated (hGH, or
pit-hGH). Manufactured growth hormone is made by recombinant DNA
technology. This is a system of genetically modifying either bacteria
cells or mammalian cells in tissue culture so that they include in their
genome, the gene that directs the cell to make human growth hormone. As
the cells in the tissue culture grow and function, they will synthesize
human growth hormone by the exact same process in the human pituitary.
Since this is a natural process, human growth hormone is not considered
a synthetic. The proper abbreviation for manufactured (recombinant)
human growth hormone is rGH. Unfortunately, the abbreviations have been
misused even in the medical community, and recombinant human growth
hormone is commonly represented by the abbreviation hGH. The designation
is no longer critical since human growth hormone of pituitary origin is
no longer used in the United States, or anywhere in the world that I'm
aware of. The term hGH or GH therefore, refers to human growth hormone
from recombinant DNA technology. It is pure and 100% free of any
contaminants or micro-organisms.

So with this being true, in this study it suppressed exercise stimulated GH for 4 days. I don't know about it suppressing the natural sleep GH release, but it sounds as if it might.

[oswaldosalcedo]

That's rHGH though............

RECOMBINANT HUMAN GROWTH HORMONE = RHGH


RHGH=HGH

[Pinnacle]

RECOMBINANT HUMAN GROWTH HORMONE = RHGH


RHGH=HGH

EXCUSEFUCKINGME..............

[oswaldosalcedo]

[QUOTE=dans]

Quote:
Most of the research that recommends bedtime injections is aimed at the individual with a non-functioning pituitary. Children with severe growth disorders and those adults who have lost pituitary function from illness, radiation treatments, AIDS, or accidents should dose GH at bedtime so as to mimmick the natural rythyms of the healthy human endocrine system.
But those who are HRT patients and bodybuilders should not. Why? Because we retain normal GH secretions, although perhaps somewhat diminished in the older lifter. ExoGH only makes the pituitary a little "lazy" for a few hours.....it is not shut down like in testosterone supplementation. Since we produce up to 80% of our natural GH during the first 2 hours of deep sleep, why not take advantage of that and dose our exoGH at a flat time like late afternoon?
Even Genentech makes this distinction now in the instructions to physicians. They specify non-bedtime injections for HRT, bedtime for sick people. Genentech invented synthetic somatropin and holds the first FDA approval for medical use.

-----------------------------------------------------

deadly wrong, genetech invented somatrem.
lilly develop somatropin.

What is the difference between patents and exclusivity?
http://forums.steroid.com/showthread.php?t=197476

What is the difference between patents and exclusivity?

--------------------------------------------------------------------------------

Patents and exclusivity work in a similar fashion but are distinctly different from one another. Patents are granted by the patent and trademark office anywhere along the development lifeline of a drug and can encompass a wide range of claims. Exclusivity is exclusive marketing rights granted by the FDA upon approval of a drug and can run concurrently with a patent or not. exclusivity is a statuatory provision and is granted to an NDA applicant if statuatory requirements are met. See 21 C.F.R. 314.108. Exclusivity was designed to promote a balance between new drug innovation and generic drug competition.


Code of Federal Regulations]
[Title 21, Volume 5, Parts 300 to 499]
From the U.S. Government Printing Office via GPO Access
[CITE: 21CFR314.108]

[Page 146-148]

TITLE 21--FOOD AND DRUGS

DEPARTMENT OF HEALTH AND HUMAN SERVICES--Continued

PART 314--APPLICATIONS FOR FDA APPROVAL TO MARKET A NEW DRUG--Table of Contents

Subpart D--FDA Action on Applications and Abbreviated Applications

Sec. 314.108 New drug product exclusivity.

(a) Definitions. The following definitions of terms apply to this
section:
Active moiety means the molecule or ion, excluding those appended
portions of the molecule that cause the drug to be an ester, salt
(including a salt with hydrogen or coordination bonds), or other
noncovalent derivative (such as a complex, chelate, or clathrate) of the
molecule, responsible for the physiological or pharmacological action of
the drug substance.
Approved under section 505(b) means an application submitted under
section 505(b) and approved on or after October 10, 1962, or an
application that was ``deemed approved'' under section 107(c)(2) of Pub.
L. 87-781.
Clinical investigation means any experiment other than a
bioavailability
---------------------------------------------------
Patents expire 20 years from the date of filing. Many other factors can affect the duration of a patent
---------------------------------------------------
Orphan Drug (ODE) - 7 years
New Chemical (NCE)- 5 years
"Other" Exclusivity - 3 years for a "change" if criteria are met
Pediatric Exclusivity (PED) - 6 months added to existing Patents/Exclusivity
Patent Challenge – (PC) – 180 days (this exclusivity is for ANDAs only).

On June 12, 1986, Eli Lilly received orphan drug status for a variant of
this product and later filed an NDA for commercial marketing.


http://www.fda.gov/bbs/topics/ANSWERS/ANS00319.html