Cosela

Drug overview for COSELA (trilaciclib dihydrochloride):

Generic name: trilaciclib dihydrochloride (TRYE-la-SYE-klib)
Drug class: Antineoplastic- Cyclin-Dependent Kinase (CDK) 4/6 Inhibitors
Therapeutic class: Antineoplastics

Trilaciclib dihydrochloride, a kinase inhibitor, is a myeloprotective agent.

No enhanced Uses information available for this drug.

DRUG IMAGES

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The following indications for COSELA (trilaciclib dihydrochloride) have been approved by the FDA:

Indications:
Prevention of chemotherapy-induced myelosuppression in extensive-stage small cell lung cancer

Professional Synonyms:
Myelopreservation in patient receiving chemotherapy for extensive-stage small cell lung cancer
Preserve bone marrow in patient receiving chemotherapy for extensive-stage small cell lung cancer
Prevention of myelosuppression due to chemotherapy in extensive-stage small cell lung cancer
Reduction of bone marrow suppression due to chemotherapy in extensive-stage small cell lung cancer

The following dosing information is available for COSELA (trilaciclib dihydrochloride):

Dosing
Administration
COSELA
Generic

Dosage of trilaciclib dihydrochloride is expressed in terms of trilaciclib.

Discontinue, withhold, or modify trilaciclib administration to manage specific adverse reactions as outlined below (see Table 1).

Table 1: Dosage Modification Recommendations for Adverse Reactions.

Adverse Reaction Severity Grade Recommendation Injection site reactions Grade 1: tenderness with Grade 1: Interrupt or including phlebitis and or without symptoms slow infusion; if 0.9% thrombophlebitis (e.g., warmth, erythema, sodium chloride is being itching) Grade 2: pain, used as a diluent/flush, lipodystrophy, edema, consider changing to 5% phlebitis Grade 3: dextrose as appropriate ulceration or necrosis, for subsequent infusions severe tissue damage, Grade 2: Interrupt operative intervention infusion; if pain is not indicated OR Grade 4: severe, follow life-threatening instructions for grade consequences 1. Ot ; urgent interventions herwise, stop infusion indicated in extremity and rotate site of infusion to site in alternative extremity.

If 0.9% sodium chloride is being used as a diluent/flush, consider changing to 5% dextrose as appropriate for subsequent infusions; central access may also b e considered Grade 3 or 4: Stop infusion and permanently discontinue Acute drug Grade 2: moderate; Grade 2: Stop infusion hypersensitivity minimal, local, or and hold until recovery reactions noninvasive intervention to grade 1 or less or indicated; limiting baseline, then consider activities of daily resuming; if grade 2 living (ADL) Grade 3: recurs, permanently severe or medically discontinue Grade 3 or significant but not 4: Permanently immediately discontinue life-threatening; hospitalization or prolongation of hospitalization indicate d; disabling; limiting self-care ADL OR Grade 4: life-threatening consequences; urgent intervention indicated Interstitial lung Grade 2 (symptomatic) Grade 2: Hold until disease/pneumonitis Grade 3: severe recovery to grade 1 or symptoms; limiting less or baseline, then self-care ADL; oxygen consider resuming; if indicated OR Grade 4: grade 2 recurs, life-threatening permanently discontinue respiratory compromise; Grade 3 or 4: urgent intervention Permanently discontinue indicated (e.g., tracheotomy, intubation) Other toxicities Grade 3: severe or Grade 3: Hold until medically significant recovery to grade 1 or but not immediately lower or baseline, then life-threatening; consider resuming; if hospitalization or grade 3 recurs, prolongation of permanently discontinue hospitalization Grade 4: Permanently indicated; disabling; discontinue limiting self-care ADL Grade 4: life-threatening consequences; urgent intervention indicated

Trilaciclib is administered by IV infusion. The drug is commercially available as a lyophilized powder that must be reconstituted and further diluted prior to IV infusion. Administer the diluted solution with an infusion set, including an in-line filter (0.2 or 0.22 micron); compatible in-line filters include polyethersulfone, polyvinylidene fluoride, and cellulose acetate.

Do not administer the solution with a polytetrafluorethylene (PTFE) in-line filter as it is incompatible; PTFE is acceptable for use in air vent filters. Do not coadminister other drugs through the same infusion line, or through a central access device unless the device supports coadministration of incompatible drugs. After the infusion is complete, flush the infusion line/cannula with >=20 mL of sterile 0.9%

sodium chloride or 5% dextrose injection. If a trilaciclib dose is missed, discontinue chemotherapy on the day the dose was missed. Consider resuming both trilaciclib and chemotherapy on the next scheduled chemotherapy day.

If trilaciclib is discontinued, wait 96 hours from the last trilaciclib dose before resuming chemotherapy only. Store unopened vials of trilaciclib at 20-25oC (excursions permitted between 15-30oC).

Dosing information for COSELA
DRUG LABEL	DOSING TYPE	DOSING INSTRUCTIONS
COSELA 300 MG VIAL	Maintenance	Adults infuse 240 mg/m2 over 30 minute(s) by intravenous route once within 4 hours prior to the start of chemotherapy

No generic dosing information available.

The following drug interaction information is available for COSELA (trilaciclib dihydrochloride):

Contraindicated
Severe
Moderate

There are 1 contraindications. These drug combinations generally should not be dispensed or administered to the same patient. A manufacturer label warning that indicates the contraindication warrants inclusion of a drug combination in this category, regardless of clinical evidence or lack of clinical evidence to support the contraindication.

Drug Interaction	Drug Names
Dofetilide/OCT2 Inhibitors SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of dofetilide by OCT2 in the kidneys.(1) CLINICAL EFFECTS: Concurrent use of OCT2 inhibitors may result in increased levels of and toxicities of dofetilide, including potentially life-threatening cardiac arrhythmias, like torsades de pointes (TdP).(1-3) PREDISPOSING FACTORS: Risk factors for QT prolongation include: cardiovascular disease (e.g. heart failure, recent myocardial infarction, history of torsades de pointes, congenital long QT syndrome), female sex, hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, advanced age, and concurrent use of agents known to cause QT prolongation.(2) Concurrent use of more than one drug known to cause QT prolongation or higher systemic concentrations of either QT prolonging drug are additional risk factors for torsades de pointes. Factors which may increase systemic drug concentrations include rapid infusion of an intravenous dose or impaired metabolism or elimination of the drug (e.g. coadministration with an agent which inhibits its metabolism or elimination, genetic impairment in drug metabolism or elimination, and/or renal/hepatic dysfunction).(2) Renal impairment may increase risk for excessive QTc prolongation as dofetilide is primarily renally eliminated. To prevent increased serum levels and risk for ventricular arrhythmias, dofetilide must be dose adjusted for creatinine clearance < or = to 60 mL/min.(1) PATIENT MANAGEMENT: The manufacturer of dofetilide states that all renal cation transport inhibitors are contraindicated. If dofetilide is to be discontinued, a washout of at least 2 days is recommended prior to starting OCT2 inhibitors.(1) If concurrent therapy is warranted, consider obtaining serum calcium, magnesium, and potassium levels and monitoring ECG at baseline and at regular intervals. Correct any electrolyte abnormalities. Instruct patients to report any irregular heartbeat, dizziness, or fainting. DISCUSSION: Dofetilide is primarily excreted in the urine via both glomerular filtration and active tubular secretion via the cation transport system. The concurrent administration of dofetilide (500 mcg twice daily) with cimetidine (an OCT2 inhibitor)(400 mg twice daily) resulted in an increase in dofetilide plasma levels by 58%. The concurrent administration of dofetilide (500 mcg single dose) with cimetidine (100 mg twice daily) resulted in an increase in dofetilide plasma levels by 13%.(1) In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(3) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively. Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(4) OCT2 inhibitors linked to this monograph include: abemaciclib, arimoclomol, givinostat, isavuconazole, trilaciclib, tucatinib, and vimseltinib. (5)	DOFETILIDE, TIKOSYN

Drug Interaction

Drug Names

Dofetilide/OCT2 Inhibitors

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of dofetilide by OCT2 in the kidneys.(1)

CLINICAL EFFECTS: Concurrent use of OCT2 inhibitors may result in increased levels of and toxicities of dofetilide, including potentially life-threatening cardiac arrhythmias, like torsades de pointes (TdP).(1-3)

PREDISPOSING FACTORS: Risk factors for QT prolongation include: cardiovascular disease (e.g. heart failure, recent myocardial infarction, history of torsades de pointes, congenital long QT syndrome), female sex, hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, advanced age, and concurrent use of agents known to cause QT prolongation.(2) Concurrent use of more than one drug known to cause QT prolongation or higher systemic concentrations of either QT prolonging drug are additional risk factors for torsades de pointes. Factors which may increase systemic drug concentrations include rapid infusion of an intravenous dose or impaired metabolism or elimination of the drug (e.g. coadministration with an agent which inhibits its metabolism or elimination, genetic impairment in drug metabolism or elimination, and/or renal/hepatic dysfunction).(2)

Renal impairment may increase risk for excessive QTc prolongation as dofetilide is primarily renally eliminated. To prevent increased serum levels and risk for ventricular arrhythmias, dofetilide must be dose adjusted for creatinine clearance < or = to 60 mL/min.(1)

PATIENT MANAGEMENT: The manufacturer of dofetilide states that all renal cation transport inhibitors are contraindicated. If dofetilide is to be discontinued, a washout of at least 2 days is recommended prior to starting OCT2 inhibitors.(1) If concurrent therapy is warranted, consider obtaining serum calcium, magnesium, and potassium levels and monitoring ECG at baseline and at regular intervals.

Correct any electrolyte abnormalities. Instruct patients to report any irregular heartbeat, dizziness, or fainting.

DISCUSSION: Dofetilide is primarily excreted in the urine via both glomerular filtration and active tubular secretion via the cation transport system. The concurrent administration of dofetilide (500 mcg twice daily) with cimetidine (an OCT2 inhibitor)(400 mg twice daily) resulted in an increase in dofetilide plasma levels by 58%. The concurrent administration of dofetilide (500 mcg single dose) with cimetidine (100 mg twice daily) resulted in an increase in dofetilide plasma levels by 13%.(1)

In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(3) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively.

Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(4) OCT2 inhibitors linked to this monograph include: abemaciclib, arimoclomol, givinostat, isavuconazole, trilaciclib, tucatinib, and vimseltinib. (5)

DOFETILIDE, TIKOSYN

There are 0 severe interactions.

There are 5 moderate interactions. The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.

Drug Interaction	Drug Names
Dalfampridine/OCT2 Inhibitors SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of dalfampridine by OCT2 in the kidneys.(1,2) CLINICAL EFFECTS: Concurrent use of OCT2 renal transport inhibitors may result in increased levels of and toxicity from dalfampridine.(1,2) PREDISPOSING FACTORS: The risk of seizures from dalfampridine may be increased in patients with a history of head trauma or prior seizure; CNS tumor; CNS infections; severe hepatic cirrhosis; excessive use of alcohol or sedatives; addiction to opiates, cocaine, or stimulants; use of over-the-counter stimulants and anorectics; diabetics treated with oral hypoglycemics or insulin; or with concomitant medications known to lower seizure threshold (antidepressants, theophylline, systemic steroids). PATIENT MANAGEMENT: Consider the potential benefits against the risks of concurrent use of dalfampridine with OCT2 renal transport inhibitors. If concurrent use is appropriate, monitor for toxicities of dalfampridine and consider dosage reduction of dalfampridine.(1,2) DISCUSSION: In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(1) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively. Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(2) OCT2 inhibitors linked to this monograph include: abemaciclib, arimoclomol, bictegravir, givinostat, isavuconazole, ranolazine, trilaciclib, trimethoprim, tucatinib, and vimseltinib.(3)	4-AMINOPYRIDINE, AMPYRA, DALFAMPRIDINE, DALFAMPRIDINE ER
Cisplatin/OCT2 Inhibitors SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of cisplatin by OCT2 in the kidneys.(1,2) CLINICAL EFFECTS: Concurrent use of OCT2 renal transport inhibitors may result in increased levels of and toxicities from cisplatin, including nephrotoxicity, ototoxicity, neuropathy, and myelosuppression.(1,2) PREDISPOSING FACTORS: Pre-existing renal insufficiency, advanced age, and dehydration may increase the risk of nephrotoxicity. PATIENT MANAGEMENT: Consider the potential benefits against the risks of concurrent use of cisplatin with OCT2 renal transport inhibitors. If concurrent use is appropriate, monitor closely for toxicities of cisplatin and consider dosage reduction of cisplatin.(1,2) DISCUSSION: In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(1) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively. Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(2) OCT2 inhibitors linked to this monograph include: abemaciclib, arimoclomol, bictegravir, dolutegravir, givinostat, isavuconazole, ranolazine, trilaciclib, trimethoprim, tucatinib, and vimseltinib.(3)	CISPLATIN, KEMOPLAT
Clofarabine/OCT2 Inhibitors SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of clofarabine by OCT2 in the kidneys.(1,2) CLINICAL EFFECTS: Concurrent use of OCT2 renal transport inhibitors may result in increased levels of and toxicity from clofarabine, including myelosuppression, serious hemorrhages, enterocolitis, nephrotoxicity, and hepatotoxicity.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Consider the potential benefits against the risks of concurrent use of clofarabine with OCT2 renal transport inhibitors. If concurrent use is appropriate, monitor for toxicities of the clofarabine and consider dosage reduction of clofarabine.(1) DISCUSSION: In an animal study, cimetidine, an OCT2 inhibitor, decreased the clearance of clofarabine in rats by 61%. The clinical implications of this finding are unclear.(1,2) In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(3) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively. Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(4) OCT2 inhibitors linked to this monograph include: abemaciclib, arimoclomol, bictegravir, cimetidine, dolutegravir, givinostat, isavuconazole, ranolazine, trilaciclib, trimethoprim, tucatinib, and vimseltinib.(5)	CLOFARABINE
Procainamide/OCT2 Inhibitors SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of procainamide by OCT2 in the kidneys.(1,2) CLINICAL EFFECTS: Concurrent use of OCT2 renal transport inhibitors may result in increased levels of and toxicities of procainamide,(1,2) including potentially life-threatening cardiac arrhythmias, like torsades de pointes (TdP).(3) PREDISPOSING FACTORS: Risk factors for QT prolongation include: cardiovascular disease (e.g. heart failure, recent myocardial infarction, history of torsades de pointes, congenital long QT syndrome), female sex, hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, advanced age, and concurrent use of agents known to cause QT prolongation.(3) Concurrent use of more than one drug known to cause QT prolongation or higher systemic concentrations of either QT prolonging drug are additional risk factors for torsades de pointes. Factors which may increase systemic drug concentrations include rapid infusion of an intravenous dose or impaired metabolism or elimination of the drug (e.g. coadministration with an agent which inhibits its metabolism or elimination, genetic impairment in drug metabolism or elimination, and/or renal/hepatic dysfunction).(3) PATIENT MANAGEMENT: Consider the potential benefits against the risks of concurrent use of procainamide with OCT2 renal transport inhibitors. If concurrent use is appropriate, monitor for toxicities of procainamide and consider dosage reduction of procainamide.(1) If concurrent therapy is warranted, consider obtaining serum calcium, magnesium, and potassium levels and monitoring ECG at baseline and at regular intervals. Correct any electrolyte abnormalities. Instruct patients to report any irregular heartbeat, dizziness, or fainting. DISCUSSION: In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(1) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively. Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(2) OCT2 inhibitors linked to this monograph include: abemaciclib, arimoclomol, bictegravir, cimetidine, dolutegravir, givinostat, isavuconazole, trilaciclib, tucatinib, and vimseltinib.(4)	PROCAINAMIDE HCL
Oxaliplatin/OCT2 Inhibitors SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Agents that inhibit the organic cation transporter 2 (OCT2) may inhibit the excretion of oxaliplatin by OCT2 in the kidneys.(1) CLINICAL EFFECTS: Concurrent use of OCT2 renal transport inhibitors may result in increased levels of and toxicity from oxaliplatin, including myelosuppression and potentially life-threatening cardiac arrhythmias, including torsades de pointes (TdP).(1) PREDISPOSING FACTORS: Risk factors for QT prolongation include: cardiovascular disease (e.g. heart failure, recent myocardial infarction, history of torsades de pointes, congenital long QT syndrome), female sex, hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, advanced age, and concurrent use of agents known to cause QT prolongation.(2) Concurrent use of more than one drug known to cause QT prolongation or higher systemic concentrations of either QT prolonging drug are additional risk factors for torsades de pointes. Factors which may increase systemic drug concentrations include rapid infusion of an intravenous dose or impaired metabolism or elimination of the drug (e.g. coadministration with an agent which inhibits its metabolism or elimination, genetic impairment in drug metabolism or elimination, and/or renal/hepatic dysfunction).(2) PATIENT MANAGEMENT: Consider the potential benefits against the risks of concurrent use of oxaliplatin with OCT2 renal transport inhibitors. If concurrent use is appropriate, monitor for toxicities of oxaliplatin and consider dosage reduction.(1) If concurrent therapy is warranted, consider obtaining serum calcium, magnesium, and potassium levels and monitoring ECG at baseline and at regular intervals. Correct any electrolyte abnormalities. Instruct patients to report any irregular heartbeat, dizziness, or fainting. DISCUSSION: In a study, givinostat increased the levels of creatinine (OCT2 substrate) by 4.76 umol/L from baseline.(3) In a study, trilaciclib increased the area-under-curve (AUC) and maximum concentration (Cmax) of metformin (an OCT2, MATE1, and MATE-2K substrate) by approximately 65% and 81%, respectively. Renal clearance of metformin was decreased by 37%. Trilaciclib did not cause significant changes in the pharmacokinetics of topotecan (a MATE1 and MATE-2K substrate).(4) OCT2 inhibitors linked to this monograph include: arimoclomol, dolutegravir, givinostat, trilaciclib, and vimseltinib.(5)	OXALIPLATIN

The following contraindication information is available for COSELA (trilaciclib dihydrochloride):

Overview
Contraindicated
Severe
Moderate

Drug contraindication overview.

*History of serious hypersensitivity reactions to trilaciclib, including anaphylaxis.

There are 1 contraindications. Absolute contraindication.

Contraindication List
Lactation

There are 5 severe contraindications. Adequate patient monitoring is recommended for safer drug use.

Severe List
Child-pugh class B hepatic impairment
Child-pugh class C hepatic impairment
Disease of liver
Interstitial lung disease
Pregnancy

There are 0 moderate contraindications.

The following adverse reaction information is available for COSELA (trilaciclib dihydrochloride):

Overview
Severe
Less Severe

Adverse reaction overview.

The most common adverse effects of trilaciclib (in >=10% of patients with >=2% difference in incidence compared to placebo in clinical studies) were fatigue, headache, pneumonia, hypocalcemia, hypokalemia, hypophosphatemia, and increased AST.

There are 9 severe adverse reactions.

More Frequent	Less Frequent
Hypokalemia Hypophosphatemia Increased aspartate transaminase Pneumonia	Hypersensitivity drug reaction Thrombophlebitis Thrombotic disorder

Rare/Very Rare
Anaphylaxis Interstitial pneumonitis

There are 11 less severe adverse reactions.

More Frequent	Less Frequent
Fatigue Headache disorder Hypocalcemia	Facial edema Hyperglycemia Injection site sequelae Peripheral edema Phlebitis after infusion Skin rash Upper abdominal pain Urticaria

Rare/Very Rare
None.

The following precautions are available for COSELA (trilaciclib dihydrochloride):

Pediatric
Pregnant
Lactation
Geriatric

Safety and efficacy of trilaciclib in pediatric patients have not been established.

Contraindicated

None

Severe Precaution

None

Management or Monitoring Precaution

None

Trilaciclib use during pregnancy can cause fetal harm based on the mechanism of action of the drug. There are no available human or animal data on trilaciclib use during pregnancy to assess the drug-associated risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes. Perform pregnancy testing in females of reproductive potential prior to initiating trilaciclib. Advise pregnant women of the potential risk to a fetus.

It is unknown whether trilaciclib distributes into human or animal milk, or affects milk production or the breast-fed infant. Because of the potential for serious adverse reactions in breast-fed infants, advise women to not breast-feed during treatment and for >=3 weeks after the last trilaciclib dose.

The manufacturer makes no specific dosage recommendations for geriatric patients. In pooled data from clinical studies, 46% of included patients who received trilaciclib were >=65 years of age. There were no overall differences in the safety or efficacy of trilaciclib between geriatric and younger patients. No clinically important differences in trilaciclib pharmacokinetics were observed based on age (range, 19-80 years).

The following icd codes are available for COSELA (trilaciclib dihydrochloride)'s list of indications:

Prevent chemotherapy-induced myelosuppression in ESCLC
C34	Malignant neoplasm of bronchus and lung
C34.0	Malignant neoplasm of main bronchus
C34.00	Malignant neoplasm of unspecified main bronchus
C34.01	Malignant neoplasm of right main bronchus
C34.02	Malignant neoplasm of left main bronchus
C34.1	Malignant neoplasm of upper lobe, bronchus or lung
C34.10	Malignant neoplasm of upper lobe, unspecified bronchus or lung
C34.11	Malignant neoplasm of upper lobe, right bronchus or lung
C34.12	Malignant neoplasm of upper lobe, left bronchus or lung
C34.2	Malignant neoplasm of middle lobe, bronchus or lung
C34.3	Malignant neoplasm of lower lobe, bronchus or lung
C34.30	Malignant neoplasm of lower lobe, unspecified bronchus or lung
C34.31	Malignant neoplasm of lower lobe, right bronchus or lung
C34.32	Malignant neoplasm of lower lobe, left bronchus or lung
C34.8	Malignant neoplasm of overlapping sites of bronchus and lung
C34.80	Malignant neoplasm of overlapping sites of unspecified bronchus and lung
C34.81	Malignant neoplasm of overlapping sites of right bronchus and lung
C34.82	Malignant neoplasm of overlapping sites of left bronchus and lung
C34.9	Malignant neoplasm of unspecified part of bronchus or lung
C34.90	Malignant neoplasm of unspecified part of unspecified bronchus or lung
C34.91	Malignant neoplasm of unspecified part of right bronchus or lung
C34.92	Malignant neoplasm of unspecified part of left bronchus or lung