CARDIZEM

CARDIZEM^®
(diltiazem hydrochloride)
Direct Compression Tablets

DESCRIPTION

CARDIZEM^® (diltiazem hydrochloride) is a calcium ion influx inhibitor (slow channel blocker or calcium antagonist). Chemically, diltiazem hydrochloride is 1, 5-Benzothiazepin-4(5H)one,3-(acetyloxy)-5-[2-(dimethyl-amino)ethyl]-2,3-dihydro-2-(4-methoxyphenyl)-, monohydrochloride,(+)-cis-. The chemical structure is:

Diltiazem hydrochloride is a white to off-white crystalline powder with a bitter taste. It is soluble in water, methanol, and chloroform. It has a molecular weight of 450.98. Each tablet of CARDIZEM contains 30 mg, 60 mg, 90 mg, or 120 mg diltiazem hydrochloride.

Also contains: D&C Yellow #10 Aluminum Lake, FD&C Yellow #6 Aluminum Lake (60 mg and 120 mg), FD&C Blue #1 Aluminum Lake (30 mg and 90 mg), hypromellose, lactose, magnesium stearate, methylparaben, microcrystalline cellulose, silicon dioxide and other ingredients.

For oral administration.

CLINICAL PHARMACOLOGY

The therapeutic benefits achieved with CARDIZEM are believed to be related to its ability to inhibit the influx of calcium ions during membrane depolarization of cardiac and vascular smooth muscle.

Mechanisms of Action

Although precise mechanisms of its antianginal action are still being delineated, CARDIZEM is believed to act in the following ways:

• 1.Angina Due to Coronary Artery Spasm. CARDIZEM has been shown to be a potent dilator of coronary arteries both epicardial and subendocardial. Spontaneous and ergonovine-induced coronary artery spasm are inhibited by CARDIZEM.
• 2.Exertional Angina. CARDIZEM has been shown to produce increases in exercise tolerance, probably due to its ability to reduce myocardial oxygen demand. This is accomplished via reductions in heart rate and systemic blood pressure at submaximal and maximal exercise workloads.

In animal models, diltiazem interferes with the slow inward (depolarizing) current in excitable tissue. It causes excitation-contraction uncoupling in various myocardial tissues without changes in the configuration of the action potential. Diltiazem produces relaxation of coronary vascular smooth muscle and dilation of both large and small coronary arteries at drug levels which cause little or no negative inotropic effect. The resultant increases in coronary blood flow (epicardial and subendocardial) occur in ischemic and nonischemic models and are accompanied by dose-dependent decreases in systemic blood pressure and decreases in peripheral resistance.

Hemodynamic and Electrophysiologic Effects

Like other calcium antagonists, diltiazem decreases sinoatrial and atrioventricular conduction in isolated tissues and has a negative inotropic effect in isolated preparations. In the intact animal, prolongation of the AH interval can be seen at higher doses.

In man, diltiazem prevents spontaneous and ergonovine-provoked coronary artery spasm. It causes a decrease in peripheral vascular resistance and a modest fall in blood pressure and, in exercise tolerance studies in patients with ischemic heart disease, reduces the heart rate-blood pressure product for any given workload. Studies to date, primarily in patients with good ventricular function, have not revealed evidence of a negative inotropic effect; cardiac output, ejection fraction, and left ventricular end-diastolic pressure have not been affected. There are as yet few data on the interaction of diltiazem and beta-blockers. Resting heart rate is usually unchanged or slightly reduced by diltiazem.

Intravenous diltiazem in doses of 20 mg prolongs AH conduction time and AV node functional and effective refractory periods approximately 20%. In a study involving single oral doses of 300 mg of CARDIZEM in six normal volunteers, the average maximum PR prolongation was 14% with no instances of greater than first-degree AV block. Diltiazem-associated prolongation of the AH interval is not more pronounced in patients with first-degree heart block. In patients with sick sinus syndrome, diltiazem significantly prolongs sinus cycle length (up to 50% in some cases).

Chronic oral administration of CARDIZEM in doses of up to 240 mg/day has resulted in small increases in PR interval, but has not usually produced abnormal prolongation.

Pharmacokinetics and Metabolism

Diltiazem is well absorbed from the gastrointestinal tract and is subject to an extensive first-pass effect, giving an absolute bioavailability (compared to intravenous dosing) of about 40%. CARDIZEM undergoes extensive metabolism in which 2% to 4% of the unchanged drug appears in the urine. In vitro binding studies show CARDIZEM is 70% to 80% bound to plasma proteins. Competitive in vitro ligand binding studies have also shown CARDIZEM binding is not altered by therapeutic concentrations of digoxin, hydrochlorothiazide, phenylbutazone, propranolol, salicylic acid, or warfarin. The plasma elimination half-life following single or multiple drug administration is approximately 3.0 to 4.5 hours. Desacetyl diltiazem is also present in the plasma at levels of 10% to 20% of the parent drug and is 25% to 50% as potent as a coronary vasodilator as diltiazem. Minimum therapeutic plasma levels of CARDIZEM appear to be in the range of 50-200 ng/mL. There is a departure from linearity when dose strengths are increased. A study that compared patients with normal hepatic function to patients with cirrhosis found an increase in half-life and a 69% increase in AUC (area-under-the-plasma concentration vs time curve) in the hepatically impaired patients. A single study in nine patients with severely impaired renal functions showed no difference in the pharmacokinetic profile of diltiazem as compared to patients with normal renal function.

CARDIZEM Tablets. Diltiazem is absorbed from the tablet formulation to about 98% of a reference solution. Single oral doses of 30 to 120 mg of CARDIZEM tablets result in detectable plasma levels within 30 to 60 minutes and peak plasma levels 2 to 4 hours after drug administration. As the dose of CARDIZEM tablets is increased from a daily dose of 120 mg (30 mg qid) to 240 mg (60 mg qid) daily, there is an increase in area-under-the-curve of 2.3 times. When the dose is increased from 240 mg to 360 mg, daily, there is an increase in area-under-the-curve of 1.8 times.

INDICATIONS AND USAGE

CARDIZEM is indicated for the management of chronic stable angina and angina due to coronary artery spasm.

CONTRAINDICATIONS

CARDIZEM is contraindicated in (1) patients with sick sinus syndrome except in the presence of a functioning ventricular pacemaker, (2) patients with second- or third-degree AV block except in the presence of a functioning ventricular pacemaker, (3) patients with hypotension (less than 90 mm Hg systolic), (4) patients who have demonstrated hypersensitivity to the drug, and (5) patients with acute myocardial infarction and pulmonary congestion documented by x-ray on admission.

WARNINGS

1. Cardiac Conduction. CARDIZEM prolongs AV node refractory periods without significantly prolonging sinus node recovery time, except in patients with sick sinus syndrome. This effect may rarely result in abnormally slow heart rates (particularly in patients with sick sinus syndrome) or second- or third-degree AV block (six of 1243 patients for 0.48%). Concomitant use of diltiazem with beta-blockers or digitalis may result in additive effects on cardiac conduction. A patient with Prinzmetal's angina developed periods of asystole (2 to 5 seconds) after a single dose of 60 mg of diltiazem. (See ADVERSE REACTIONS section.)

2. Congestive Heart Failure. Although diltiazem has a negative inotropic effect in isolated animal tissue preparations, hemodynamic studies in humans with normal ventricular function have not shown a reduction in cardiac index nor consistent negative effects on contractility (dp/dt). Experience with the use of CARDIZEM alone or in combination with beta-blockers in patients with impaired ventricular function is very limited. Caution should be exercised when using the drug in such patients.

3. Hypotension. Decreases in blood pressure associated with CARDIZEM therapy may occasionally result in symptomatic hypotension.

4. Acute Hepatic Injury. In rare instances, significant elevations in enzymes such as alkaline phosphatase, LDH, SGOT, SGPT, and other phenomena consistent with acute hepatic injury have been noted. These reactions have been reversible upon discontinuation of drug therapy. The relationship to CARDIZEM is uncertain in most cases, but probable in some. (See PRECAUTIONS.)

PRECAUTIONS

General

CARDIZEM (diltiazem hydrochloride) is extensively metabolized by the liver and excreted by the kidneys and in bile. As with any drug given over prolonged periods, laboratory parameters of renal and hepatic function should be monitored at regular intervals. The drug should be used with caution in patients with impaired renal or hepatic function. In subacute and chronic dog and rat studies designed to produce toxicity, high doses of diltiazem were associated with hepatic damage. In special subacute hepatic studies, oral doses of 125 mg/kg and higher in rats were associated with histological changes in the liver, which were reversible when the drug was discontinued, in dogs, doses of 20 mg/kg were also associated with hepatic changes; however, these changes were reversible with continued dosing. Dermatological events (see ADVERSE REACTIONS section) may be transient and may disappear despite continued use of CARDIZEM. However, skin eruptions progressing to erythema multiforme and/or exfoliative dermatitis have also been infrequently reported. Should a dermatologic reaction persist, the drug should be discontinued.

Drug Interactions

Due to the potential for additive effects, caution and careful titration are warranted in patients receiving CARDIZEM concomitantly with any agents known to affect cardiac contractility and/or conduction. (See WARNINGS.)

Pharmacologic studies indicate that there may be additive effects in prolonging AV conduction when using beta-blockers or digitalis concomitantly with CARDIZEM. (See WARNINGS.)

As with all drugs, care should be exercised when treating patients with multiple medications. Diltiazem is both a substrate and an inhibitor of the cytochrome P-450 3A4 enzyme system. Other drugs that are specific substrates, inhibitors, or inducers of this enzyme system may have a significant impact on the efficacy and side effect profile of diltiazem. Patients taking other drugs that are substrates of CYP450 3A4, especially patients with renal and/or hepatic impairment, may require dosage adjustment when starting or stopping concomitantly administered diltiazem in order to maintain optimum therapeutic blood levels.

Carcinogenesis, Mutagenesis, Impairment of Fertility

A 24-month study in rats and a 21-month study in mice showed no evidence of carcinogenicity. There was also no mutagenic response in in vitro bacterial tests. No intrinsic effect on fertility was observed in rats.

Pregnancy

Nursing Mothers

Diltiazem is excreted in human milk. One report suggests that concentrations in breast milk may approximate serum levels. If use of CARDIZEM is deemed essential, an alternative method of infant feeding should be instituted.

Pediatric Use

Safety and effectiveness in pediatric patients have not been established.

Geriatric Use

Clinical studies of diltiazem did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. Other reported clinical experience has not identified differences in responses between the elderly and younger patients. In general dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.

ADVERSE REACTIONS

Serious adverse reactions have been rare in studies carried out to date, but it should be recognized that patients with impaired ventricular function and cardiac conduction abnormalities usually have been excluded.

In domestic placebo-controlled angina trials, the incidence of adverse reactions reported during CARDIZEM therapy was not greater than that reported during placebo therapy.

The following represent occurrences observed in clinical studies of angina patients. In many cases, the relationship to CARDIZEM has not been established. The most common occurrences from these studies, as well their frequency of presentation, are edema (2.4%), headache (2.1%), nausea (1.9%), dizziness (1.5%), rash (1.3%), and asthenia (1.2%). In addition, the following events were reported infrequently (less than 1 %):

Cardiovascular: Angina, arrhythmia, AV block (first degree), AV block (second or third degree – see conduction warning), bradycardia bundle branch block, congestive heart failure, ECG abnormality, flushing, hypotension, palpitations, syncope, tachycardia, ventricular extrasystoles.

Nervous System: Abnormal dreams, amnesia, depression, gait abnormality, hallucinations, insomnia, nervousness, paresthesia, personality change, somnolence, tremor

Gastrointestinal: Anorexia, constipation, diarrhea, dysgeusia, dyspepsia, mild elevations of alkaline phosphatase, SGOT, SGPT, and LDH (see hepatic warnings), thirst, vomiting, weight increase

Dermatological: Petechiae, photosensitivity, pruritus, urticaria

Other: Amblyopia, CPK elevation, dry mouth, dyspnea, epistaxis, eye irritation, hyperglycemia, hyperuricemia, impotence, muscle cramps, nasal congestion, nocturia, osteoarticular pain, polyuria, sexual difficulties, tinnitus

The following postmarketing events have been reported infrequently in patients receiving CARDIZEM: allergic reactions, alopecia, angloedema (including facial or periorbital edema), asystole, erythema multiforme (including Stevens-Johnson syndrome, toxic epidermal necrolysis), extrapyramidal symptoms, gingival hyperplasia, hemolytic anemia, increased bleeding time, leukopenia, purpura, retinopathy, myopathy, and thrombocytopenia. There have been observed cases of a generalized rash, some characterized as leukocytoclastic vasculitis. In addition, events such as myocardial infarction have been observed, which are not readily distinguishable from the natural history of the disease in these patients. A definitive cause and effect relationship between these events and CARDIZEM therapy cannot yet be established. Exfoliative dermatitis (proven by rechallenge) has also been reported.

OVERDOSAGE OR EXAGGERATED RESPONSE

The oral LD₅₀s in mice and rats range from 415 to 740 mg/kg and from 560 to 810 mg/kg, respectively. The intravenous LD₅₀s in these species were 60 and 38 mg/kg, respectively. The oral LD₅₀ in dogs is considered to be in excess of 50 mg/kg, while lethality was seen in monkeys at 360 mg/kg.

The toxic dose in man is not known. Due to extensive metabolism, blood levels after a standard dose of diltiazem can vary over tenfold, limiting the usefulness of blood levels in overdose cases.

There have been reports of diltiazem overdose in amounts ranging from <1>

Events observed following diltiazem overdose included bradycardia, hypotension, heart block, and cardiac failure. Most reports of overdose described some supportive medical measure and/or drug treatment. Bradycardia frequently responded favorably to atropine, as did heart block, although cardiac pacing was also frequently utilized to treat heart block. Fluids and vasopressors were used to maintain blood pressure and in cases of cardiac failure inotropic agents were administered. In addition, some patients received treatment with ventilatory support, gastric lavage, activated charcoal, and/or intravenous calcium.

The effectiveness of intravenous calcium administration to reverse the pharmacological effects of diltiazem overdose has been inconsistent. In a few reported cases, overdose with calcium channel blockers associated with hypotension and bradycardia that was initially refractory to atropine became more responsive to after the patients received intravenous calcium. In some cases intravenous calcium has been administered (1 g calcium chloride or 3 g calcium gluconate) over 5 minutes, and repeated every 10-20 minutes as necessary. Calcium gluconate has also been administered as a continuous infusion at a rate of 2 g per hour for 10 hours. Infusions of calcium for 24 hours or more may be required. Patients should be monitored for signs of hypercalcemia.

In the event of overdose or exaggerated response, appropriate supportive measures should be employed in addition to gastrointestinal decontamination. Diltiazem does not appear to be removed by peritoneal or hemodialysis. Limited data suggest that plasmapheresis or charcoal hemoperfusion may hasten diltiazem elimination following overdose. Based on the known pharmacological effects of diltiazem and/or reported clinical experiences, the following measures may be considered:

Bradycardia: Administer atropine (0.60 to 1.0 mg). If there is no response to vagal blockade, administer isoproterenol cautiously.

High-Degree AV Block: Treat as for bradycardia above. Fixed high-degree AV block should be treated with cardiac pacing.

Cardiac Failure: Administer inotropic agents (isoproterenol, dopamine, or dobutamine) and diuretics.

Hypotension: Vasopressors (eg, dopamine or levarterenol bitartrate).

Actual treatment and dosage should depend on the severity of the clinical situation and the judgment and experience of the treating physician.

DOSAGE AND ADMINISTRATION

Exertional Angina Pectoris Due to Atherosclerotic Coronary Artery Disease or Angina Pectoris at Rest Due to Coronary Artery Spasm

Dosage must be adjusted to each patient's needs. Starting with 30 mg four times daily, before meals, and at bedtime, dosage should be increased gradually (given in divided doses three or four times daily) at 1- to 2-day intervals until optimum response is obtained. Although individual patients may respond to any dosage level, the average optimum dosage range appears to be 180 to 360 mg/day. There are no available data concerning dosage requirements in patients with impaired renal or hepatic function. If the drug must be used in such patients, titration should be carried out with particular caution.

Concomitant Use With Other Cardiovascular Agents

• 1.Sublingual NTG may be taken as required to abort acute anginal attacks during CARDIZEM (diltiazem hydrochloride) therapy.
• 2.Prophylactic Nitrate Therapy. CARDIZEM may be safely coadministered with short- and long-acting nitrates, but there have been no controlled studies to evaluate the antianginal effectiveness of this combination.
• 3.Beta-blockers. (See WARNINGS and PRECAUTIONS.)

HOW SUPPLIED

CARDIZEM 30-mg tablets are supplied in bottles of 100 (NDC 64455-771-47) and 500 (NDC 64455-771-55). Each green tablet is engraved with MARION on one side and 1771 on the other.

CARDIZEM 60-mg scored tablets are supplied in bottles of 100 (NDC 64455-772-47) and 500 (NDC 64455-772-55). Each yellow tablet is engraved with MARION on one side and 1772 on the other.

CARDIZEM 90-mg scored tablets are supplied in bottles of 100 (NDC 64455-791-47). Each green oblong tablet is engraved with CARDIZEM on one side and 90 mg on the other.

CARDIZEM 120-mg scored tablets are supplied in bottles of 100 (NDC 64455-792-47). Each yellow oblong tablet is engraved with CARDIZEM on one side and 120 mg on the other.

Store at 25°C (77°); excursions permitted to 15-30°C (59-86°) [see USP Controlled Room Temperature].

Avoid excessive humidity.

Prescribing Information as of August 2001

®Cardizem is a registered trademark of Biovail Laboratories Incorporated

Manufactured by:
Aventis Pharmaceuticals Inc.
Kansas City, MO, 64137, USA

Distributed by:
Biovail Pharmaceuticals, Inc.
Bridgewater, NJ, 08807, USA

50070671

Medical drugs

FDA Exclusive Enforcement, Lanham Act Division

The Ninth Circuit just issued a major decision reaffirming the principle that FDA exclusive enforcement powers prohibit plaintiffs from bringing what amount to private FDCA violation claims in the guise of private civil litigation. See Photomedex, Inc. v. Irwin, No. 07-56672, slip op. (9th Cir. April 15, 2010).


First, an aside. Are we reading that number right? This is a 2007appeal? We’ve heard criticism that the Ninth Circuit has become too big and ponderous, but we never thought about it all that much – being on the opposite coast. Well, if the Ninth Circuit’s got a three-year appeal backlog, that’s just too much, and something really ought to be done to divide that court in half, or some other approach. Justice delayed is justice denied, and so on and so forth…. Is the Ninth Circuit simply to big to succeed?

But back to the main point.

We’ve gone on until we’re blue in the face about how 21 U.S.C. §337(a) represents express congressional policy that nobody but the government (that is, the Department of Justice or the FDA) can seek to enforce the Food, Drug and Cosmetic Act (“FDCA”) in a court of law. We’d list some posts, but there are, frankly, too many of them, so here’s the search results for “337(a).”

The no-private-right-of-action argument is especially important in dealing with negligence per se claims and the so-called “parallel violation” claims that are essentially the only avenue arguably left open to plaintiffs in Class III PMA medical device cases afterRiegel v. Medtronic, Inc., 552 U.S. 312 (2008).

But the issue also comes up in Lanham Act cases involving litigation between commercial competitors. Indeed, when Bexis first got the idea to put the §337(a) argument to work in the personal injury field over a decade ago in the Bone Screwlitigation, Lanham Act cases were the primary source of available precedent.

They continue to be valuable precedent today. Photomedexinvolved a dispute between competing manufacturers of different lasers used for treating skin diseases (psoriasis, etc.). The founder of the defendant company used to work for the plaintiff company, which no doubt added a bit of personal animosity to the mix. The plaintiff made the usual potpourri of claims, but the important one for our purposes was the Lanham Act claim that the defendants sought commercial advantage by misrepresenting that the FDA had cleared (lasers are not PMA devices) their competing laser. Photomedex, slip op. at 5544-45 (9th Circuit pagination is obviously unusual, as the first page here is 5539)

Because the Lanham Act is a federal statute, Photomedex, unlikeBuckman Co. v. Plaintiffs’ Legal Committee, 531 U.S. 341 (2001), which involved state-law claims, there’s no preemption argument. But the flip side of preemption where exclusive FDA enforcement is concerned, is standing. The Court accepted that, in any kind of suit, §337(a) restricts the ability of a plaintiff to pursue a theory that turns on claimed FDCA violations:

Section 337(a) of the FDCA bars private enforcement of the statute, stating that “all such proceedings for the enforcement, or to restrain violations, of this [Act] shall be by and in the name of the United States.” The Supreme Court has observed that Section 337(a) “leaves no doubt that it is the Federal Government rather than private litigants who are authorized to file suit for noncompliance with the medical device provisions.” Buckman, 531 U.S. at 349 n. 4.

The Supreme Court made clear in Buckman that this section also limits the ability of a private plaintiff to pursue claims under state law theories where such claims collide with the exclusive enforcement power of the federal government. Id. at 343, 349-50, 353 (holding that a state tort claim based on alleged fraudulent representations made by a medical device manufacturer in the course of seeking market approval from the FDA “would exert an extraneous pull on the scheme established by Congress, and it is therefore pre-empted by that scheme”).

Slip op. at 5547-47 (citations omitted). Where the FDA has not found a violation, no private party can assert that there is one. “Because the FDCA forbids private rights of action under that statute, a private action brought under the Lanham Act may not be pursued when, as here, the claim would require litigation of the alleged underlying FDCA violation in a circumstance where the FDA has not itself concluded that there was such a violation.” Id. at 5548.

The Photomedex court carved out a familiar exception – that a flat out yes/no misrepresentation of FDA approval would escape §337(a). Id. (“an affirmative statement of approval by the FDA” where “no such FDA approval had been granted” may be pursued). But that sort of yes/no situation, where examination of the underlying regulatory scheme was unnecessary, wasn’t what happened in this case.

Rather, the plaintiff’s FDA approval (technically “clearance,” seeslip op. at 5550 n.3, distinguishing between “approval” and “clearance”) claim would have required a court to delve into the intricacies of the FDA’s “minor modification” rule. That is, it involved whether modifications to an already cleared device were sufficiently “major” to require the submission of a whole new §510k submission under 21 C.F.R. §807.81(a)(3). Slip op. at 5550-51. Whether the device that the defendant sold was a "major" modification of the device that the FDA had previously cleared could not be determined without examining the application of the FDA’s regulatory scheme to the facts:

It is significant that under the regulatory structure established by the FDA for the medical devices at issue in this case, clearance to market a given device did not necessarily require an affirmative statement of approval by the FDA. The FDA’s previous clearance of the [device that the defendant licensed] covered Defendants’ . . . device as well, as long as [it] was not significantly modified from the [prior] device.

Slip op. at 5551. Determining whether modifications were “minor” was “the responsibility in the first instance” of the device manufacturer. Id. Although the court doesn’t dig that far into the facts, presumably the defendant had the necessary minor modification memo in its files.

So the underlying legal dispute boiled down to the plaintiff claiming that the defendant’s device didn’t really have FDA clearance/approval because it wasn’t really a minor modification of the cleared product that the defendant had licensed. Slip op. at 5551-52. That sunk pretty far into FDCA minutiae, and (it seems to us obviously) would have required examination of whether the FDA would find a violation.

Indeed, the plaintiff more or less cut its own throat in this regard, as it actually filed some sort of “complaint” with the FDA that led to an FDA investigation of the issue. The defendant gave the FDA agent a copy of what we presume was its minor modification memo (although the court does not use this term), and the FDA closed its investigation without finding its violation. Slip op. at 5552-53. The significance of the plaintiff's actions did not escape the court's attention. “That [plaintiff] engaged in an extensive campaign to try to convince the FDA to act on [defendant’s] supposed misstatements and violations demonstrates that [plaintiff] understood that this subject fell within the FDA’s domain.” Id. at 5559.

Please note, we've only given a stripped down version of the facts, and the actual FDA proceedings, which included a supplemental submission seeking clearance of additional uses, were much more involved. See slip op. at 5552-54. All those details may be fodder for the FDA Law Blog, but from our perspective, they only make the rubble bounce. We’re only concerned with the proposition that private plaintiffs can’t enforce purported FDCA violations, a point that’s readily transferrable to the tort sandbox where we play.

What we like is this: “The statute assigns to the FDA the responsibility for taking enforcement action against Defendants.” Slip op. at 5554. And this: “[Plaintiff] is not permitted to circumvent the FDA’s exclusive enforcement authority by seeking to prove that Defendants violated the FDCA, when the FDA did not reach that conclusion.” Id. And this: “[I]t is impossible for [plaintiff] to prove that [defendant’s] device had not been cleared by the FDA when the FDA itself did not take that position.” Id.

As we said above, other Lanham Act cases have taken pretty much the same position – since before the Bone Screw litigation that began in the mid 1990s. The court in Photomedex cites a bunch of these cases: IQ Products Co. v. Pennzoil Products Co., 305 F.3d 368, 372-74 (5th Cir. 2002) (not an FDCA case); Dial A Car, Inc. v. Transportation, Inc., 82 F.3d 484, 488-90 (D.C. Cir. 1996) (not an FDCA case); Mylan Laboratories, Inc. v. Matkari, 7 F.3d 1130, 1139 (4th Cir. 1993); Sandoz Pharmaceuticals Corp. v. Richardson-Vicks, Inc., 902 F.2d 222, 230-32 (3d Cir. 1990);Summit Technology, Inc. v. High-Line Medical Instruments Co., 933 F. Supp. 918, 934 (C.D. Cal. 1996); Summit Technology, Inc. v. High-Line Medical Instruments Co., 922 F. Supp. 299, 305-07 (C.D. Cal. 1996). See Slip op. at 5555-56.

Significantly, the Photomedex court discussed and distinguishedAlpharma, Inc. v. Pennfield Oil Co., 411 F.3d 934 (8th Cir. 2005), which dealt with FDA-approved uses for animal feed additives. The court found that Alpharma was much more of a straight yes/no case on FDA approval, since in Alpharma “the FDA made it clear that there was no record of the defendant obtaining the FDA’s approval for the additional uses." Photomedex, slip op. at 5557.

If you want a bunch more cases – all of which involve the FDCA – see our prior post on “What To Do With Un-Preempted Fraud On The FDA Claims.” If you’re still not satisfied, you’ll just have to buy Bexis’ book, which discusses the Lanham Act precedent in §4.02[2] and footnotes literally dozens of cases (Bexis has always been funny that way). Anyway, we’re sure Bexis will be adding this one to his book, since the court concludes:

The FDCA explicitly says that enforcement power is reserved to the federal government. To permit [plaintiff] to proceed with a claim that Defendants violated this law when the FDA did not so determine would, in effect, permit [plaintiff] to assume enforcement power which the statute does not allow and require the finder of fact to make a decision that the FDA itself did not make. We therefore affirm the order of summary judgment for the claims based on Defendants’ statements that the [device] had FDA clearance.

Photomedex, slip op. at 5559.

Photomedex is the first time the Ninth Circuit has spoken on the issue of FDA enforcement exclusivity and itsl preclusive effect on private litigation of supposed violations. While the opinion did not discuss state law because the plaintiff conceded it couldn’t pursue its consumer fraud claims, slip op. at 5559 n.7, other plaintiffs have not been so reasonable. Thus, the recognition inPhotomedex of the §337(a) exclusivity will be extremely useful precedent against plaintiffs bringing negligence per se/"parallel violation" claims, as we’ve already discussed here, as well as against plaintiffs seeking to bring economic loss claims under federal statutes such as RICO, as we already discussed here.

So if you’re facing a claim of any sort – be it statutory or common law – where the guts of the plaintiff’s arguments are that your client somehow violated the FDCA, you’ll want to read, and probably want to cite, Photomedex.