ATNAA ATROPINE AND PRALIDOXIME CHLORIDE AUTO-INJECTOR - atropine and pralidoxime chloride

United States - English - NLM (National Library of Medicine)

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Active ingredient:
atropine (UNII: 7C0697DR9I) (atropine - UNII:7C0697DR9I)
Available from:
Meridian Medical Technologies, Inc.
INN (International Name):
atropine
Composition:
atropine 2.1 mg in 0.7 mL
Administration route:
INTRAMUSCULAR
Prescription type:
PRESCRIPTION DRUG
Therapeutic indications:
The ATNAA is indicated for the treatment of poisoning by susceptible organophosphorous nerve agents having anticholinesterase activity. In the face of life-threatening poisoning by organophosphorous nerve agents, there are no absolute contraindications for the use of the ATNAA (see WARNINGS ). Atropine and pralidoxime chloride are not subject to abuse and possess no known potential for dependence.
Product summary:
The Antidote Treatment – Nerve Agent, Auto-Injector (ATNAA) provides Atropine Injection (atropine, 2.1 mg/0.7 mL) and Pralidoxime Chloride Injection (pralidoxime chloride, 600 mg/2 mL) in sterile solutions for intramuscular injection. The ATNAA is a self-contained unit designed for automatic self- or buddy-administration by military personnel. ATNAAs are supplied through the Directorate of Medical Materiel, Defense Supply Center, Philadelphia. Store at 25°C (77°F); excursions permitted to 15 - 30°C (59 - 86°F) [see USP Controlled Room Temperature] Keep from Freezing. Protect from Light. Manufactured by: MERIDIAN MEDICAL TECHNOLOGIES® , INC. A wholly-owned subsidiary of King Pharmaceuticals® , Inc. 0001566 4/10 Rx only.
Authorization status:
New Drug Application
Authorization number:
11704-777-01

ATNAA ATROPINE AND PRALIDOXIME CHLORIDE AUTO-INJECTOR - atropine and

pralidoxime chloride

Meridian Medical Technologies, Inc.

----------

“ATNAA”

(ANTIDOTE TREATMENT – NERVE AGENT, AUTO-INJECTOR) ATROPINE

INJECTION, 2.1 mg/0.7 mL

PRALIDOXIME CHLORIDE INJECTION, 600 mg/2 mL FOR USE IN NERVE AGENT

POISONING ONLY

STERILE SOLUTIONS FOR INTRAMUSCULAR USE ONLY

DESCRIPTION

The Antidote Treatment - Nerve Agent, Auto-Injector (ATNAA) provides Atropine Injection and

Pralidoxime Chloride Injection in separate chambers as sterile, pyrogen-free solutions for

intramuscular injection.

The ATNAA is a specially designed unit for automatic self- or buddy-administration by military

personnel. When activated, the ATNAA sequentially administers atropine and pralidoxime chloride

through a single needle. The recommended procedure (see DOSAGE AND ADMINISTRATION) is

to inject the contents of the auto-injector into the muscles of an outer thigh or into the buttocks.

When activated, each ATNAA dispenses:

2.1 mg atropine in 0.7 mL of a sterile, pyrogen-free solution containing 12.47 mg glycerin and not more

than 2.8 mg phenol, citrate buffer, and Water for Injection. The pH range is 4.0 – 5.0.

600 mg of pralidoxime chloride in 2 mL of a sterile, pyrogen-free solution containing 40 mg benzyl

alcohol, 22.5 mg glycine, and Water for Injection. The pH is adjusted with hydrochloric acid. The pH

range is 2.0 – 3.0.

After an ATNAA has been activated, the empty container should be disposed of properly (see

DOSAGE AND ADMINISTRATION). It cannot be refilled, nor can the protruding needle be

retracted.

Atropine, an anticholinergic agent (muscarinic antagonist), occurs as white crystals, usually needle-

like, or as a white, crystalline powder. It is slightly soluble in water, soluble in glycerin and ether, and

freely soluble in alcohol and chloroform with a molecular weight of 289.38. Atropine, a naturally

occurring belladonna alkaloid, is a racemic mixture of equal parts of d- and l- hyoscyamine, whose

activity is due almost entirely to the levo isomer of the drug. Chemically, atropine is designated as

1αH,5αH-Tropan-3α-ol (±)-tropate. Its empirical formula is C

H NO and its structural formula is:

Pralidoxime chloride, a cholinesterase reactivator, is an odorless, white to pale-yellow crystalline

powder, freely soluble in water, with a molecular weight of 172.61. Chemically, pralidoxime chloride

is designated as 2-formyl-1-methylpyridinium chloride oxime. Its empirical formula is C H CIN O and

its structural formula is:

The specific activity of the drug resides in the 2-formyl-1-methylpyridinium ion and is independent of

the particular salt employed. The chloride salt is preferred because of physiologic compatibility,

excellent water solubility at all temperatures, and high potency per gram, due to its low molecular

weight.

CLINICAL PHARMACOLOGY

Mechanism of Action:

Atropine

Atropine is commonly classified as an anticholinergic or antiparasympathetic (parasympatholytic) drug.

More precisely, however, it is termed an antimuscarinic agent since it antagonizes the muscarine-like

actions of acetylcholine and other choline esters.

Atropine inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic

cholinergic nerves, and on smooth muscles which respond to endogenous acetylcholine but are not so

innervated. As with other antimuscarinic agents, the major action of atropine is a competitive or

surmountable antagonism which can be overcome by increasing the concentration of acetylcholine at

receptor sites of the effector organ (e.g., by using anticholinesterase agents which inhibit the enzymatic

destruction of acetylcholine). The receptors antagonized by atropine are the peripheral structures that

are stimulated or inhibited by muscarine, (i.e., exocrine glands and smooth and cardiac muscle).

Responses to postganglionic cholinergic nerve stimulation may also be inhibited by atropine but this

occurs less readily than with responses to injected (exogenous) choline esters.

Pralidoxime Chloride

The principal action of pralidoxime is to reactivate cholinesterase (mainly outside the central nervous

system) which has been inactivated by phosphorylation due to an organophosphorous nerve agent or

related compound, although pralidoxime does not reactivate cholinesterase inactivated by all

organophosphate nerve agents (e.g. soman). The destruction of accumulated acetylcholine can then

proceed and neuromuscular junctions will again function normally. Pralidoxime also slows the process

of “aging” of phosphorylated cholinesterase to a non-reactivatable form and detoxifies certain

organophosphates by direct chemical reaction.

Pharmacodynamics :

Atropine

Atropine reduces secretions in the mouth and respiratory passages, relieves the constriction and spasm

of the respiratory passages, and may reduce the paralysis of respiration which results from actions of

the toxic agent on the central nervous system. Atropine-induced parasympathetic inhibition may be

preceded by a transient phase of stimulation, especially on the heart where small doses first slow the

rate before characteristic tachycardia develops due to paralysis of vagal control. Although mild vagal

excitation occurs, the increased respiratory rate and occasionally increased depth of respiration

produced by atropine are more probably the result of bronchiolar dilatation. Accordingly, atropine is an

unreliable respiratory stimulant and large or repeated doses may depress respiration.

Adequate doses of atropine abolish various types of reflex vagal cardiac slowing or asystole. The

drug also prevents or abolishes bradycardia or asystole produced by injection of choline esters,

anticholinesterase agents or other parasympathomimetic drugs, and cardiac arrest produced by

stimulation of the vagus. Atropine may also lessen the degree of partial heart block when vagal activity

is an etiologic factor. In some patients with complete heart block, the idioventricular rate may be

accelerated by atropine; in others, the rate is stabilized. Occasionally, a large dose may cause

atrioventricular (A-V) block and nodal rhythm.

Atropine in clinical doses counteracts the peripheral dilatation and abrupt decrease in blood pressure

produced by choline esters. However, when given by itself, atropine does not exert a striking or

uniform effect on blood vessels or blood pressure. Systemic doses slightly raise systolic and lower

diastolic pressures and can produce significant postural hypotension. Such doses also slightly increase

cardiac output and decrease central venous pressure. Occasionally, therapeutic doses dilate cutaneous

blood vessels, particularly in the “blush” area (atropine flush), and may cause atropine “fever” due to

suppression of sweat gland activity in infants and small children.

Pralidoxime Chloride

Pralidoxime chloride has its most critical effect in relieving paralysis of the muscles of respiration.

Because pralidoxime is less effective in relieving depression of the respiratory center, atropine is

always required concomitantly to block the effect of accumulated acetylcholine at this site.

Pralidoxime relieves muscarinic signs and symptoms, salivation, bronchospasm, etc., but this action is

relatively unimportant since atropine is adequate for this purpose.

Published reports have established the safety and efficacy of atropine and pralidoxime chloride used

separately, as well as the safety and increased efficacy of atropine and pralidoxime chloride when

administered concomitantly in the treatment of nerve agent poisoning in humans .

Pharmacokinetics :

Atropine

Atropine is rapidly and well absorbed after intramuscular administration. Atropine disappears rapidly

from the blood and is distributed throughout the various body tissues and fluids. Much of the drug is

destroyed by enzymatic hydrolysis, particularly in the liver; from 13 to 50% is excreted unchanged in

the urine. Traces are found in various secretions, including milk. Atropine readily crosses the placental

barrier and enters the fetal circulation.

The C

, and T of atropine following 2.09 mg atropine given intramuscularly by multi-

chambered delivery system was 13 ± 3 ng/mL, 31 ± 30 minutes, and 2.4 ± 0.3 hours, respectively. The

protein binding of atropine is 14 to 22% in plasma. There are gender differences in the

pharmacokinetics of atropine. The AUC

and C

were 15% higher in females than males. The

half-life of atropine is slightly shorter (approximately 20 minutes) in females than males.

Pralidoxime Chloride

Pralidoxime is distributed throughout the extracellular water; it is not bound to plasma protein. The drug

is rapidly excreted in the urine partly unchanged, and partly as a metabolite produced by the liver.

Consequently, pralidoxime is relatively short acting and repeated doses may be needed, especially

where there is any evidence of continuing absorption of the poison.

The C

and T½ of pralidoxime following 600 mg pralidoxime given intramuscularly by multi-

chambered delivery system was 7 ± 3 mcg/mL, 28 ± 15 minutes, and 2 ± 1 hour, respectively. The C

of pralidoxime was about 36% higher in females than males but the AUC was comparable between the

two genders.

INDICATIONS AND USAGE

(0-inf)

The ATNAA is indicated for the treatment of poisoning by susceptible organophosphorous nerve

agents having anticholinesterase activity.

CONTRAINDICATIONS

In the face of life-threatening poisoning by organophosphorous nerve agents, there are no absolute

contraindications for the use of the ATNAA (see WARNINGS).

WARNINGS

While ATNAA can be administered to all individuals with a life-threatening exposure to

organophosphorous nerve agents, it should be administered with extreme caution to individuals with the

following disorders when the symptoms of nerve agent poisoning are less severe: individuals who are

hypersensitive to any component of the product, disorders of heart rhythm such as atrial flutter, severe

narrow angle glaucoma, pyloric stenosis, or prostatic hypertrophy.

More than one dose of ATNAA, to a maximum of three doses, may be necessary, especially when

exposure is massive or symptoms are severe (see DOSAGE AND ADMINISTRATION). Children

are more susceptible than adults to the toxic effects of anticholinergic agents.

Severe difficulty in breathing requires artificial respiration in addition to the use of the ATNAA.

Pralidoxime is not effective in the treatment of poisoning due to phosphorus, inorganic phosphates, or

organophosphates not having anticholinesterase activity.

PRECAUTIONS

General: The desperate condition of the organophosphorous-poisoned patient will generally mask such

minor signs and symptoms of atropine and pralidoxime treatment as have been noted in normal subjects.

Because pralidoxime is excreted in the urine, a decrease in renal function will result in increased blood

levels of the drug.

The ATNAA should be used with caution in all individuals over 40 years of age. Conventional

systemic doses may precipitate acute glaucoma in susceptible patients, convert partial organic pyloric

stenosis into complete pyloric obstruction, precipitate urinary retention in patients with prostatic

hypertrophy, or cause inspiration of bronchial secretions and formation of dangerous viscid plugs in

patients with chronic lung disease.

Information for Patients: Appropriate steps must be taken to insure that personnel understand the

indications for, and use of, the ATNAA, including review of symptoms of poisoning and operation of

the ATNAA (see DOSAGE AND ADMINISTRATION and Patient Instruction Sheet).

Drug Interactions: When atropine and pralidoxime are used together, the signs of atropinization

(flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than might be

expected when atropine is used alone because pralidoxime may potentiate the effect of atropine.

The following precautions should be kept in mind in the treatment of anticholinesterase poisoning,

although they do not bear directly on the use of atropine and pralidoxime. Since barbiturates are

potentiated by the anticholinesterases, they should be used cautiously in the treatment of convulsions.

Morphine, theophylline, aminophylline, succinylcholine, reserpine, and phenothiazine- type

tranquilizers should be avoided in treating personnel with organophosphorous poisoning.

Carcinogenesis, Mutagenesis, Impairment of Fertility: No reports regarding the potential of

atropine or pralidoxime chloride for carcinogenesis, mutagenesis, or impairment of fertility have been

published in the literature. Since the ATNAA is indicated for short-term emergency use only, no

investigations of these aspects have been conducted.

2,3,4

Pregnancy: Teratogenic Effects - Pregnancy Category C: Adequate animal reproduction studies

have not been conducted with atropine, pralidoxime, or the combination. It is not known whether

pralidoxime or atropine can cause fetal harm when administered to a pregnant woman or if these agents

can affect reproductive capacity. The ATNAA should be administered to a pregnant woman only if

clearly needed.

Nursing Mothers: It is not known whether these drugs are excreted in human milk. Because many drugs

are excreted in human milk, caution should be exercised when the ATNAA is administered to a nursing

woman.

Pediatric Use: Safety and effectiveness in pediatric patients have not been established.

ADVERSE REACTIONS

Mild to moderate pain may be experienced at the site of injection.

Atropine

The major side effects of atropine can be attributed to antimuscarinic action. These include dryness of

the mouth, blurred vision, photophobia, confusion, headache, dizziness, tachycardia, palpitations,

flushing, urinary hesitance or retention, constipation, abdominal distention, nausea, vomiting, loss of

libido, and impotency. Anhidrosis may produce heat intolerance and impairment of temperature

regulation in a hot environment. Larger or toxic doses may produce such central effects as restlessness,

tremor, fatigue, locomotor difficulties, delirium, followed by hallucinations, depression,

and ultimately, medullary paralysis and death. Large doses can also lead to circulatory collapse. In such

cases, blood pressure declines and death due to respiratory failure may ensue following paralysis and

coma. Hypersensitivity reactions will occasionally occur with atropine; these are usually seen as skin

rashes, on occasion progressing to exfoliation.

Pralidoxime Chloride

Pralidoxime may cause blurred vision, diplopia and impaired accommodation, dizziness, headache,

drowsiness, nausea, tachycardia, increased systolic and diastolic blood pressure, hyperventilation,

decreased renal function, and muscular weakness when given parenterally to normal volunteers who

have not been exposed to anticholinesterase poisons. In actual cases of poisoning, it is very difficult to

differentiate some of the toxic effects produced by atropine or the organophosphate compound from

those of pralidoxime chloride.

Excitement and manic behavior immediately following recovery of consciousness after

organophosphorous poisoning treated with pralidoxime chloride have been reported in several cases.

However, similar behavior has occurred in cases that were not treated with pralidoxime.

Elevations in SGOT and/or SGPT enzyme levels were observed in one of six normal volunteers given

1200 mg of pralidoxime chloride intramuscularly, and in 4 of 6 volunteers given 1800 mg

intramuscularly. Levels returned to normal in about two weeks.

Transient elevations in creatine phosphokinase were observed in all normal volunteers given the drug.

A single intramuscular injection of 330 mg in 1 mL in rabbits caused myonecrosis, inflammation, and

hemorrhage.

Atropine and Pralidoxime Chloride

When atropine and pralidoxime are used together, the signs of atropinization may occur earlier than

might be expected when atropine is used alone.

DRUG ABUSE AND DEPENDENCE

Atropine and pralidoxime chloride are not subject to abuse and possess no known potential for

3,5,6

dependence.

OVERDOSAGE

Symptoms :

Atropine

Serious overdosage with atropine is characterized by widespread paralysis of parasympathetically

innervated organs. Dry mucous membranes, widely dilated and nonresponsive pupils, tachycardia, fever,

and cutaneous flush are especially prominent, as are mental and neurological symptoms.

Disorientation, mania, hallucinations, gait disturbances, and symptoms may last 48 hours or longer. In

instances of severe intoxication, respiratory depression, coma, circulatory collapse, and death may

occur.

The fatal dose of atropine is not known. In the treatment of organophosphorous poisoning, 200 mg

doses have been used and doses as high as 1000 mg have been given.

In children, 10 mg or less may be fatal. With a dose as low as 0.5 mg, undesirable minimal symptoms or

responses of overdosage may occur. These increase in severity and extent with larger doses of the

drug (excitement, hallucinations, delirium, and coma with a dose of 10 mg or more). However, in the

presence of organophosphate poisoning, higher doses of atropine may be tolerated.

Pralidoxime Chloride

Symptoms of pralidoxime chloride overdose have been observed in normal subjects only: dizziness,

blurred vision, diplopia, headache, impaired accommodation, nausea, slight tachycardia. In therapy it has

been difficult to differentiate side effects due to the drug from those due to effects of the poison.

Treatment:

Supportive treatment should be administered as indicated. If respiration is depressed, artificial

respiration with oxygen is necessary. Ice bags, alcohol sponges or a hypothermia blanket may be

required to reduce fever, especially in children. Catheterization may be necessary if urinary retention

occurs. Since atropine elimination takes place through the kidney, urinary output must be maintained and

increased if possible; intravenous fluids may be indicated. Because of the affected person's

photophobia, the room should be darkened.

In the event of toxic overdosage, a short acting barbiturate or diazepam may be given as needed to

control marked excitement and convulsions. Large doses for sedation should be avoided because

central depressant action may coincide with the depression occurring late in atropine poisoning.

Central stimulants are not recommended. Physostigmine, given as an atropine antidote by slow

intravenous injection of 1 to 4 mg (0.5 to 1.0 mg in children), rapidly abolishes delirium and coma

caused by large doses of atropine. Since physostigmine has a short duration of action, the patient may

again lapse into coma after one or two hours and repeated doses are likely to be required.

Neostigmine, pilocarpine, and methacholine are of little real benefit, since they do not penetrate the

blood-brain barrier.

DOSAGE AND ADMINISTRATION

For optimal reactivation of organophosphorous-inhibited cholinesterase, the ATNAA should be

administered as soon as possible after appearance of symptoms of nerve agent poisoning (see below).

The ATNAA should be self- or buddy–administered by military personnel after donning protective

mask and hood at the first sign of a chemical attack, and only if some or all of the following mild

symptoms of nerve agent exposure are present:

The following are the instructions that should be given to military personnel.

Self-Aid

1. Administer one (1) ATNAA into your lateral thigh muscle or buttocks as follows:

a. Remove gray safety cap from back end.

b. Place front end on outer thigh and push hard until injector functions. Hold firmly in place for ten

seconds.

c. Using a hard surface, bend needle into hook. Push ejected needle through a pocket flap (or other

thick and conspicuous part of outer clothing).

2. Wait 10 to 15 minutes for the antidote to take effect. If you are able to ambulate, know who you are,

and where you are, you will NOT need a second injection. Warning: Giving yourself a second set

of injections may cause an overdose of the ATNAA which could result in incapacitation.

3. If symptoms of nerve agent poisoning are not relieved after administering one injection, seek

someone else to check your symptoms. A buddy must administer the second and third injections, if

needed.

Buddy-Aid

1. Casualties with severe symptoms may experience most or all of the mild symptoms described above,

plus most or all of the following:

2. If you encounter a service member suffering from severe signs of nerve agent poisoning, render the

following aid:

a. Mask the casualty, if necessary. Do not fasten the hood.

b. If self-aid (one ATNAA) has been administered, administer in rapid succession two (2)

additional ATNAAs into the casualty's lateral thigh muscle or buttocks.

Note: Use the casualty's own ATNAAs when providing aid. Do not use your own injectors on a

Unexplained runny nose

Unexplained sudden headache

Sudden drooling

Difficulty in seeing (dimness of vision and miosis)

Tightness of chest or difficulty in breathing

Wheezing and coughing

Localized sweating and muscular twitching in the area of contaminated skin

Stomach cramps

Nausea, with or without vomiting

Tachycardia followed by bradycardia

Strange or confused behavior

Increased wheezing and increased difficulty in breathing

Severely pinpointed pupils

Red eyes with tearing

Vomiting

Severe muscular twitching and general weakness

Involuntary urination and defecation

Convulsions

Unconsciousness

Respiratory failure

Bradycardia

casualty. If you do, you may not have any antidote available when needed for self- aid.

c. If self-aid (one ATNAA) has not been administered, administer in rapid succession three (3)

ATNAAs into the casualty's lateral thigh muscle or buttocks.

IMPORTANT: PHYSICIANS AND/OR MEDICAL PERSONNEL ASSISTING EVACUATED

VICTIMS OF NERVE AGENTS, SHOULD AVOID EXPOSING THEMSELVES TO

CONTAMINATION BY THE VICTIM'S CLOTHING.

HOW SUPPLIED

The Antidote Treatment – Nerve Agent, Auto-Injector (ATNAA) provides Atropine Injection (atropine,

2.1 mg/0.7 mL) and Pralidoxime Chloride Injection (pralidoxime chloride, 600 mg/2 mL) in sterile

solutions for intramuscular injection. The ATNAA is a self-contained unit designed for automatic self-

or buddy-administration by military personnel. ATNAAs are supplied through the Directorate of

Medical Materiel, Defense Supply Center, Philadelphia.

Store at 25°C (77°F); excursions permitted to 15 - 30°C (59 - 86°F)

[see USP Controlled Room Temperature]

Keep from Freezing. Protect from Light.

Manufactured by:

MERIDIAN MEDICAL TECHNOLOGIES , INC.

A wholly-owned subsidiary of King Pharmaceuticals

, Inc.

0001566

4/10

Rx only.

REFERENCES

1. Landauer, W: Cholinomimetic teratogens. V. The effect of oximes and related cholinesterase

reactivators. Teratology 15: 33 (Feb) 1977.

2. Moller, K.O., Jensen-Holm, J. and Lausen, H.H.: Ugeskr Laeg. 123: 501, 1961.

3. Namba, T., Nolte, C.T., Jackrel, J. and Grob, D.: Poisoning due to organophosphate insecticides.

Acute and chronic manifestations. Amer. J. Med. 50: 475 (Apr), 1971.

4. Arena, J.M.: Poisoning, Toxicology Symptoms, Treatments, ed. 4, Springfield, IL, Charles C.

Thomas, 1979, p. 133.

5. Brachfeld, J., and Zavon, M.R.: Organic phosphate (Phosdrin®) Intoxication. Report of a case and

the results of treatment with 2-PAM, Arch. Environ. Health 11:859, 1965.

6. Hayes, W.J., Jr.: Toxicology of Pesticides. Baltimore, The Williams & Wilkins Company, 1975, p.

416.

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

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

Principal Display Panel

ANTIDOTE TREATMENT NERVE AGENT, AUTO-INJECTOR

For Use in Nerve Agent Poisoning Only

ATROPINE INJECTION 2.1 MG,

PRALIDOXIME CHLORIDE INJECTION 600MG

MERIDIAN MEDICAL TECHNOLOGIES

Columbia, MD 21046, USA

A Pfizer Company.

ATNAA Utilizes Binaject

Technology 0001860

Sterile Solution for Intramuscular Use Only

NSN 6505-01-362-7427

NDC 11704-777-01

Rx Only

Store at 25°C (77°F); excursions permitted to 15 - 30°C (59-86°F).

Keep From Freezing. Protect From Light.

ATNAA ATROPINE AND PRALIDOXIME CHLORIDE AUTO-INJECTOR

atropine and pralidoxime chloride kit

Product Information

®

®

Product T ype

HUMAN PRESCRIPTION DRUG

Ite m Code (Source )

NDC:1170 4-777

Packag ing

#

Item Code

Package Description

Marketing Start

Date

Marketing End

Date

1

NDC:1170 4-

777-0 1

1 in 1 CARTON; Type 2: Prefilled Drug Delivery Device/System

(syringe, patch, etc.)

0 1/17/20 0 2

Quantity of Parts

Part #

Package Quantity

Total Product Quantity

Pa rt 1

1 SYRINGE, GLASS

0 .7 mL

Pa rt 2

1 SYRINGE, GLASS

2 mL

Part 1 of 2

ATNAA ATROPINE AND PRALIDOXIME CHLORIDE AUTO-INJECTOR

atropine injection

Product Information

Route of Administration

INTRAMUSCULAR

Active Ingredient/Active Moiety

Ingredient Name

Basis of Strength

Stre ng th

a tro pine (UNII: 7C0 6 9 7DR9 I) (atro pine - UNII:7C0 6 9 7DR9 I)

a tro pine

2.1 mg in 0 .7 mL

Inactive Ingredients

Ingredient Name

Stre ng th

Glycerin (UNII: PDC6 A3C0 OX)

Citric Acid Mo no hydra te (UNII: 29 6 8 PHW8 QP)

Pheno l (UNII: 339 NCG44TV)

Wa ter (UNII: 0 59 QF0 KO0 R)

So dium Citra te (UNII: 1Q73Q2JULR)

Nitro g en (UNII: N76 29 21K75)

Packag ing

#

Item

Co de

Package Description

Marketing Start

Date

Marketing End

Date

1

0 .7 mL in 1 SYRINGE, GLASS; Type 2: Prefilled Drug Delivery Device/System

(syringe, patch, etc.)

Marketing Information

Marke ting Cate gory

Application Numbe r or Monograph Citation

Marke ting Start Date

Marke ting End Date

NDA0 21175

0 1/17/20 0 2

Part 2 of 2

ATNAA ATROPINE AND PRALIDOXIME CHLORIDE AUTO-INJECTOR

pralidoxime chloride injection

Product Information

Route of Administration

INTRAMUSCULAR

Active Ingredient/Active Moiety

Ingredient Name

Basis of Strength

Stre ng th

pra lido xime chlo ride (UNII: 38 X7XS0 76 H) (pralido xime - UNII:P7MU9 UTP52)

pralido xime chlo ride

6 0 0 mg in 2 mL

Inactive Ingredients

Ingredient Name

Stre ng th

Benzyl Alco ho l (UNII: LKG8 49 4WBH)

Glycine (UNII: TE76 6 0 XO1C)

Wa ter (UNII: 0 59 QF0 KO0 R)

Hydro chlo ric Acid (UNII: QTT1758 2CB)

Packag ing

#

Item

Co de

Package Description

Marketing Start

Date

Marketing End

Date

1

2 mL in 1 SYRINGE, GLASS; Type 2: Prefilled Drug Delivery Device/System

(syringe, patch, etc.)

Marketing Information

Marke ting Cate gory

Application Numbe r or Monograph Citation

Marke ting Start Date

Marke ting End Date

NDA0 21175

0 1/17/20 0 2

Marketing Information

Marke ting Cate gory

Application Numbe r or Monograph Citation

Marke ting Start Date

Marke ting End Date

NDA0 21175

0 1/17/20 0 2

Labeler -

Meridian Medical T echnologies, Inc. (167671341)

Meridian Medical Technologies, Inc.

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Meridian Medical Techno lo gies, Inc.

0 38 8 8 9 234

MANUFACTURE(1170 4-777) , ANALYSIS(1170 4-777)

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Meridian Medical Techno lo gies, Inc.

0 78 8 0 8 315

MANUFACTURE(1170 4-777) , LABEL(1170 4-777) , PACK(1170 4-777)

Establishment

Name

Ad d re s s

ID/FEI

Busine ss Ope rations

Meridian Medical Techno lo gies,

Inc .

16 76 71341

MANUFACTURE(1170 4-777) , LABEL(1170 4-777) , PACK(1170 4-777) ,

ANALYSIS(1170 4-777)

Revised: 3/2017

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