Bomyntra (denosumab-bnht)
Hypercalcemia Agents Subcutaneous Syringe (Ml); Subcutaneous Vial (Ml)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Denosumab, denosumab-bbdz, denosumab-bmwo, denosumab-bnht, denosumab-desu, denosumab-dssb, denosumab-kyqq, denosumab-mobz, denosumab-nxxp, and denosumab-qbde, fully human monoclonal antibodies that are specific for the receptor activator of nuclear factor kappa-B ligand (RANKL) and act as RANKL inhibitors, are bone resorption inhibitors.
FDA defines a biosimilar as a biological product that is highly similar to an FDA-licensed reference biological with the exception of minor differences in clinically inactive components and for which there are no clinically meaningful differences in safety, purity, or potency. The claim of biosimilarity is based on a totality-of-evidence approach, which includes consideration of data from analytical, animal, and clinical studies (e.g., human pharmacokinetic and pharmacodynamic studies, clinical immunogenicity assessment, additional comparative clinical studies). Therefore, biosimilarity may be established even when there are formulation or minor structural differences as long as these differences are not clinically meaningful.
Biosimilars are approved through an abbreviated licensure pathway that establishes biosimilarity between the proposed biological and the reference biological but does not independently establish safety and effectiveness of the proposed biological. In order to be considered an interchangeable biosimilar, a biological product must meet additional requirements beyond demonstrating biosimilarity to its reference product; these requirements include demonstrating that the biological product can be expected to produce the same clinical results as the reference product in any given patient and, for a biological product that is administered more than once to an individual, the risk in terms of safety or diminished efficacy of alternating or switching between use of the biological product and the reference product is no greater than the risk of using the reference product without such alteration or switch. Biosimilar products that are interchangeable can be substituted for the reference product without the intervention of the healthcare provider who prescribed the reference product.
All of the approved denosumab biosimilars have brand name products that are designated as interchangeable with denosumab (Prolia(R)) or denosumab (Xgeva(R)).
In this monograph, unless otherwise stated, the term ''denosumab products'' refers to denosumab (the reference drug) and its approved biosimilars.
Denosumab, a fully human monoclonal immunoglobulin G2 (IgG2) antibody, is a bone resorption inhibitor. The drug has affinity and specificity for human receptor activator of nuclear factor kappa-B (RANK) ligand (RANKL) and acts as a RANKL inhibitor. A member of the tumor necrosis factor (TNF) superfamily, membrane-bound RANKL is expressed by osteoblasts.
Its receptor (RANK) is expressed on the cell surfaces of osteoclasts and osteoclast precursors. The interaction between RANK and RANKL is integral to the normal bone resorption process as it promotes osteoclast differentiation and activation and inhibits osteoclast apoptosis. The actions of denosumab are similar to those of osteoprotegerin, a decoy receptor for RANKL that is principally secreted by osteoblasts and bone marrow stromal cells.
Denosumab (like osteoprotegerin) binds RANKL, preventing interaction with RANK. This inhibits osteoclast formation, function, and survival, decreasing bone resorption. In contrast to osteoprotegerin; however, denosumab is specific for RANKL and does not appear to bind to other members of the TNF superfamily.
Denosumab therapy results in reduced bone resorption markers and increased cortical and trabecular bone mass and strength. Reductions in bone formation markers are also seen, presumably due to the natural coupling of bone formation and resorption processes. The effects of denosumab are considered reversible since bone turnover markers and bone mineral density (BMD) return to baseline within 12 months after the drug is discontinued.
When rechallenged with denosumab, patients exhibit reproducible suppression of bone remodeling and increases in BMD.
In giant cell tumors of bone, stromal cells express RANKL and osteoclast-like giant cells express RANK receptor; signaling through the RANK receptor contributes to osteolysis and tumor growth. Denosumab prevents RANKL from activating the receptor on the surfaces of osteoclast, their precursors, and osteoclast-like giant cells.
Studies in postmenopausal women with osteoporosis indicate that biochemical bone turnover markers are suppressed within 3 days after a 60-mg dose of denosumab and maximal reductions generally occur by 1 month; toward the end of each 6-month dosing interval, serum concentrations of denosumab decrease with subsequent increases in bone turnover markers. The effects of denosumab on bone remodeling are thus reversible, and these effects were sustained with continued treatment.
In patients with breast cancer and bone metastases, the median reduction in urine N-telopeptide adjusted for urine creatinine (uNTx/Cr) was 82% within 1 week following the initial 120-mg dose of denosumab; in several trials in patients with bone metastases from solid tumors, the median reduction in uNTx/Cr from baseline to 3 months was approximately 80%. In patients with newly diagnosed multiple myeloma receiving subcutaneous denosumab in a dosage of 120 mg once every 4 weeks, steady-state concentrations of the drug appeared to be achieved by 6 months; the median reduction in uNTx/Cr was approximately 75% by week 5 and 74-79% during weeks 9-49 of therapy. In adults and skeletally mature adolescents with giant cell tumor of bone receiving subcutaneous denosumab in a dosage of 120 mg once every 4 weeks with a 120-mg loading dose on days 8 and 15, the median reduction in uNTx/Cr from baseline was 84% at week 13 and 82% at week 25.
Following subcutaneous administration, bioavailability of denosumab is 62%. The drug exhibits a prolonged absorption phase; the median time to peak serum concentrations after a single 60-mg subcutaneous dose is 10 days (range: 3-21 days). No drug accumulation or change in pharmacokinetics with time was observed upon multiple subcutaneous dosing of denosumab 60 mg every 6 months.
Formation of binding antibodies did not affect pharmacokinetics. In patients with bone metastases receiving subcutaneous denosumab in a dosage of 120 mg once every 4 weeks, serum denosumab concentrations accumulated up to 2.8-fold and steady state was achieved by 6 months. When administered at the recommended dosage in patients with giant cell tumor of bone (120 mg once every 4 weeks, with an additional 120-mg dose given on day 8 and day 15 during the first month), steady state was achieved in 3 months.
Characterization of other monoclonal antibodies indicates that absorption is probably mediated by the lymphatic system. Furthermore, denosumab exhibits a prolonged beta-phase and a more rapid terminal elimination phase, resulting in a mean half-life of approximately 25-28 days. Denosumab clearance is thought to occur via the reticuloendothelial system and renal excretion is not expected.
The pharmacokinetics of denosumab are not affected by age, race, or gender. The pharmacokinetics of denosumab (in a dosage of 120 mg once every 4 weeks with a 120-mg loading dose on days 8 and 15) were similar between adults and skeletally-mature adolescents with giant cell tumor of bone. Studies using denosumab in a dosage of 60 mg once every 6 months indicate that pharmacokinetics are not affected by body weight.
Studies using denosumab in a dosage of 120 mg once every 4 weeks indicate that steady-state exposure is lower in 120-kg patients compared with 66-kg patients.
Denosumab (Prolia(R)) is used in the treatment of osteoporosis in postmenopausal women and men at high risk for fracture, in the treatment of glucocorticoid-induced osteoporosis in patients at high risk for fracture, and to increase bone mass in patients at high risk for fracture who are receiving androgen deprivation or aromatase inhibitor therapy.
Generic name: denosumab-bnht
Pronunciation: (den-OH-sue-mab)
Drug class: Hypercalcemia Agents
Therapeutic class: Endocrine
Reference product & biosimilars
| Name | Biosimilar | Interchangeable |
|---|---|---|
|
Xgeva
Reference
Amgen
|
||
| Biocon Biologic | Biosimilar | Interchangeable |
| Organon Llc | Biosimilar | Interchangeable |
| Fresenius Kabi | Biosimilar | Interchangeable |
| Accord Biopharm | Biosimilar | Interchangeable |
| Celltrion Usa, | Biosimilar | Interchangeable |
| Sandoz | Biosimilar | Interchangeable |
| Hikma Pharmaceuticals USA | Biosimilar | Interchangeable |
Today’s intelligence on Bomyntra
Indications
The following indications are listed for Bomyntra:
- Giant Cell Tumor Of Bone
- Humoral Hypercalcemia Of Malignancy
- Prevention Of Skeletal Related Events Associated With Bone Metastases From Solid Tumor
- Prevention Of Skeletal Related Events In Multiple Myeloma
Also known as: Hypercalcemia Associated With Cancer, Hypercalcemia Associated With Malignancy, Hypercalcemia Of Malignancy, Malignant Hypercalcemia.
Dosing
Correct preexisting hypocalcemia prior to treatment initiation. Supplementation with calcium and vitamin D may be required during treatment. All patients treated with denosumab products for osteoporosis or bone loss indications should receive 1000 mg of calcium daily and >=400 IU of vitamin D daily.
Administer denosumab products by subcutaneous injection using single-dose prefilled syringes and/or single-use vials; refer to the prescribing information of the individual denosumab product for available dosage forms.
Subcutaneous injections of denosumab should be made into the upper arm, upper thigh, or abdomen. Do not administer IV, or by IM or intradermal injection.
Refer to the individual denosumab product labeling for storage information. Do not use after the expiration date stated on the label. Do not shake denosumab products vigorously.
| Drug label | Dosing type | Instructions |
|---|---|---|
| Bomyntra 120 Mg/1.7 Ml Vial | Maintenance | Inject 1.7 milliliters (120 mg) by subcutaneous route every 4 weeks. |
| Bomyntra 120 Mg/1.7 Ml Syringe | Maintenance | Inject 1.7 milliliters (120 mg) by subcutaneous route every 4 weeks. |
No dosing information is available for this tab.
Drug interactions
There is no enhanced messaging for this drug.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Antibody-Based Therapies/Imlifidase
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: Imlifidase is a cysteine protease that cleaves immunoglobulin G (IgG), which results in degradation of all subclasses of human and rabbit IgG. Therapies based on human or rabbit IgG may be inactivated if given concurrently with imlifidase.(1)
CLINICAL EFFECTS: Antibody therapies based on human or rabbit IgG may be inactivated and lead to decreased efficacy.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Concurrent use of imlifidase and antibody-based therapies should be closely evaluated for timing of administration to avoid decreased efficacy of the antibody-based therapy.(1) Antibody-based therapies cleaved by imlifidase include, but are not limited to, basiliximab, rituximab, alemtuzumab, adalimumab, denosumab, belatacept, etanercept, rabbit anti-human thymocyte globulin (rATG) and intravenous immunoglobulin (IVIg). The prescribing information recommends the following time intervals for administration of antibody-based therapies after administration of imlifidase: -Equine anti-thymocyte globulin: No time interval needed (may be administered concurrently) -Intravenous immunoglobulin (IVIg): 12 hours -Adalimumab, alemtuzumab, basiliximab, denosumab, etanercept, or rituximab: 4 days -Rabbit anti-human thymocyte globulin (rATG) or belatacept: 1 week In addition, IVIg may contain neutralizing antibodies against imlifidase, which may inactivate imlifidase if IVIg is given before imlifidase. Consider the half-life of IVIg (3-4 weeks) before imlifidase administration to patients treated with IVIg. Eculizumab is not cleaved by imlifidase at the recommended dose level.(1)
DISCUSSION: Imlifidase is a cysteine protease that cleaves IgG, which results in degradation of all subclasses of human and rabbit IgG. Antibody therapies based on human or rabbit IgG may be inactivated if given in connection with imlifidase.(1) IVIg may contain neutralizing antibodies against imlifidase, which may inactivate imlifidase if IVIg is given before imlifidase. In clinical studies, IVIg was not administered within 4 weeks before imlifidase infusion.(1)
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Igg Antibodies And Derivatives/Efgartigimod-Alfa
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The neonatal Fc receptor (FcRn) prevents catabolism and mediates recycling of IgG and albumin, which leads to their long persistence in the body.(1,2) Efgartigimod-alfa binds to FcRn and may decrease systemic exposure of other ligands of FcRn, like immunoglobulins and IgG-based antibodies.(3)
CLINICAL EFFECTS: The effectiveness of medicines that bind to FcRn may be decreased.(3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The manufacturer of efgartigimod-alfa states that efgartigimod-alfa should not be combined with long-term use of FcRn-binding medications. If the medication is essential for the patient, efgartigimod-alfa should be discontinued.(3)
DISCUSSION: Clinical drug interaction studies with efgartigimod-alfa have not been performed. Efgartigimod-alfa may decrease concentrations of compounds that bind to the human FcRn.(3)
Igg Antibodies And Derivatives/Nipocalimab-Aahu
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: The neonatal Fc receptor (FcRn) prevents catabolism and mediates recycling of IgG and albumin, which leads to their long persistence in the body.(1,2) Nipocalimab-aahu binds to FcRn and may decrease systemic exposure of other ligands of FcRn, like immunoglobulins and IgG-based antibodies.(3)
CLINICAL EFFECTS: The effectiveness of medicines that bind to FcRn may be decreased.(3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The manufacturer of nipocalimab-aahu states that nipocalimab-aahu should not be combined with long-term use of FcRn-binding medications. If the medication is essential for the patient, nipocalimab-aahu should be discontinued.(3)
DISCUSSION: Clinical drug interaction studies with nipocalimab-aahu have not been performed. Nipocalimab-aahu may decrease concentrations of compounds that bind to the human FcRn.(3)
Moderate Interaction: Assess the risk to the patient and take action as needed.
Igg Antibodies And Derivatives/Rozanolixizumab-Noli
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: The neonatal Fc receptor (FcRn) prevents catabolism and mediates recycling of IgG and albumin, which leads to their long persistence in the body.(1,2) Rozanolixizumab-noli binds to FcRn and may decrease systemic exposure of other ligands of FcRn, like immunoglobulins and IgG-based antibodies.(3)
CLINICAL EFFECTS: The effectiveness of medications that bind to FcRn may be decreased.(3)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The manufacturer of rozanolixizumab-noli states that concurrent use with medications that bind to the human neonatal Fc receptor (FcRn) should be closely monitored for reduced effectiveness of these medications. If long-term use of such medications is essential for the patient, consider discontinuing rozanolixizumab-noli and use alternative therapies.(3)
DISCUSSION: Clinical drug interaction studies with rozanolixizumab-noli have not been performed. Rozanolixizumab-noli may decrease concentrations of compounds that bind to the human FcRn.(3)
Contraindications
*Hypocalcemia (correct preexisting hypocalcemia prior to initiating denosumab products).
*History of clinically important hypersensitivity (e.g., systemic hypersensitivity) to denosumab products or any component in the formulation.
*Denosumab products labeled for use in the treatment of osteoporosis or bone loss (Prolia(R)) and its biosimilars are contraindicated in pregnant women.
There are no contraindication contraindications for this drug.
- Chronic kidney disease stage 4 (severe) GFR 15-29 ml/min
- Chronic kidney disease stage 5 (failure) GFr<15 ml/min
- Congenital long QT syndrome
- Hypocalcemia
- Infection
- Pregnancy
- Diabetes mellitus
- Hypoparathyroidism
- Invasive dental procedure
- Kidney disease with likely reduction in glomerular filtration rate (GFr)
- Periodontitis
- Thyroid surgery
Adverse reactions
Adverse effects reported in clinical trials in >5% of patients receiving denosumab for the treatment of osteoporosis and reported more frequently with the drug than with placebo include back pain, extremity pain, musculoskeletal pain, hypercholesterolemia, and cystitis (in postmenopausal women) or back pain, arthralgia, and nasopharyngitis (in men).
Adverse effects reported in clinical trials in >3% of patients receiving denosumab for the treatment of glucocorticoid-induced osteoporosis and reported more frequently with denosumab than with risedronate include back pain, hypertension, bronchitis, and headache.
In clinical trials in patients receiving androgen deprivation or aromatase inhibitor therapy, adverse effects reported in >=10% of patients receiving denosumab for treatment of bone loss and reported more frequently with the drug than with placebo include arthralgia and back pain. Musculoskeletal and extremity pain have also been reported.
Adverse effects reported in clinical trials in >=25% of patients with bone metastases from solid tumors receiving denosumab include fatigue/asthenia, hypophosphatemia, and nausea.
Adverse effects reported in clinical trials in >=10% of patients with multiple myeloma receiving denosumab include diarrhea, nausea, anemia, back pain, thrombocytopenia, peripheral edema, hypocalcemia, upper respiratory infection, rash, and headache.
Adverse effects reported in clinical trials in >=10% of patients receiving denosumab for treatment of giant cell tumor of bone include arthralgia, headache, nausea, back pain, fatigue, and extremity pain.
Adverse effects reported in clinical trials in >20% of patients receiving denosumab for bisphosphonate-refractory hypercalcemia of malignancy include nausea, dyspnea, decreased appetite, headache, peripheral edema, vomiting, anemia, constipation, and diarrhea.
More Frequent
- Dyspnea
Less Frequent
- Hypertension
- Hypokalemia
- Hypomagnesemia
Rare or Very Rare
- Anaphylaxis
- Angina
- Aseptic necrosis of jaw bone
- Atypical femoral fracture
- Cataracts
- Cellulitis
- Cholesteatoma of external ear
- Dental abscess
- DRESS syndrome
- Endocarditis
- Erysipelas
- Hypercalcemia
- Hyperparathyroidism
- Hypersensitivity angiitis
- Hypersensitivity drug reaction
- Hypocalcemia
- Hypotension
- Infection
- Malignancy
- Osteonecrosis of external auditory canal
- Pancreatitis
- Polymyalgia rheumatica
- Severe infection
- Throat constriction
- Vasculitis
More Frequent
- Back pain
- Fatigue
- General weakness
- Hypophosphatemia
- Musculoskeletal pain
- Nausea
- Thrombocytopenic disorder
Less Frequent
- Allergic dermatitis
- Anemia
- Anorexia
- Arthralgia
- Bone pain
- Bronchitis
- Constipation
- Cough
- Cystitis
- Diarrhea
- Dizziness
- Dyspepsia
- Eczema
- Flatulence
- Gastroesophageal reflux disease
- Headache disorder
- Hypercholesterolemia
- Infection of ear
- Insomnia
- Pain in extremities
- Peripheral edema
- Pharyngitis
- Pneumonia
- Pruritus of skin
- Sciatica
- Skin inflammation
- Skin rash
- Spinal osteoarthritis
- Upper abdominal pain
- Upper respiratory infection
- Urinary tract infection
- Vertigo
- Vomiting
Rare or Very Rare
- Alopecia
- Ear itching
- Earache
- Erythema
- Facial edema
- Hearing loss
- Herpes zoster
- Impacted cerumen
- Injection site sequelae
- Lichenoid dermatitis drug eruption
- Tinnitus
- Urticaria
Precautions
No enhanced messaging available.
Safety and efficacy of denosumab (Xgeva(R)) and its biosimilars have been established for treatment of giant cell tumor of bone in skeletally mature adolescents (12-16 years of age). Safety and efficacy of denosumab have not been established for any other indication in pediatric patients.
Safety and efficacy of denosumab (Prolia(R)) and its biosimilars have not been established in pediatric patients. Cases of hypercalcemia (some requiring hospitalization and/or complicated by acute kidney injury) have been reported in clinical trials of pediatric patients with osteogenesis imperfecta treated with denosumab. Clinical trials of denosumab in osteogenesis imperfecta were terminated early due to these life-threatening events; efficacy for this indication was not demonstrated. A small clinical trial in pediatric patients with glucocorticoid-induced osteoporosis also did not demonstrate efficacy of denosumab for this indication. In pediatric patients <4 years of age, denosumab may adversely affect long-bone growth and dentition based on evidence from animal studies.
Clinically important hypercalcemia has been reported following discontinuance of denosumab therapy in pediatric patients with growing skeletons who received the drug for treatment of giant cell tumor of bone or for other off-label uses. Based on animal data, denosumab potentially may impair bone growth in children with open growth plates and may inhibit eruption of dentition.
Based on findings from animal studies and the mechanism of action of denosumab, the drug may cause fetal harm if administered to pregnant women. Reproduction studies in monkeys have demonstrated fetal loss, stillbirth, postnatal mortality, evidence of absent lymph nodes, abnormal bone growth, reduced bone strength, reduced hematopoiesis, dental dysplasia, tooth malalignment, and decreased neonatal growth. Some of the observed bone abnormalities recovered once drug exposure ceased following birth. No evidence of maternal harm was observed prior to labor in the studies. A study in mice found that absence of receptor activator of nuclear factor kappa-B ligand (RANKL; the target of denosumab) resulted in fetal lymph node agenesis and postnatal impairment of bone growth and dentition.
Confirm pregnancy status prior to initiation of therapy in females of reproductive potential. Apprise pregnant women and females of reproductive potential of the potential drug-associated risk to the fetus.
It is not known whether denosumab is distributed into human milk; the effects of the drug on breast-fed infants or on milk production are also unknown. Denosumab is distributed into milk in monkeys in concentrations of <=0.5% of those attained in serum at <=1 month after the last dose. Studies in pregnant RANKL knockout mice indicate that denosumab exposure during pregnancy may impair maternal mammary gland development and lactation; however, no such impairment was observed in monkeys.
The manufacturers of Prolia(R)and its biosimilars recommend to not breast-feed during treatment. The manufacturers of Xgeva(R) and its biosimilars state to consider the developmental and health benefits of breast-feeding along with the mother's clinical need for treatment with a denosumab product and any potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.
The manufacturer makes no specific dosage recommendations for geriatric patients.
When the total number of patients studied in clinical trials of denosumab for osteoporosis or bone loss indications is considered, 76% were >=65 years of age, while 27% were >=75 years of age; in clinical trials in men with osteoporosis or in patients with glucocorticoid-induced osteoporosis, 55 or 47%, respectively, of patients were >=65 years of age, while 16 or 17%, respectively, were >=75 years of age.
Of the total number of patients studied in clinical trials of denosumab for cancer-related indications, 44-45% were >=65 years of age, while 16-17% were >=75 years of age.
Although no overall differences in efficacy or safety were observed between geriatric and younger patients and other clinical experience has revealed no evidence of age-related differences, the possibility that some older patients may exhibit increased sensitivity to the drug cannot be ruled out.
ICD codes
| Code | Type | Description |
|---|---|---|
| Giant cell tumor of bone | ||
| C40 | ICD10CM | Malignant neoplasm of bone and articular cartilage of limbs |
| C40.0 | ICD10CM | Malignant neoplasm of scapula and long bones of upper limb |
| C40.00 | ICD10CM | Malignant neoplasm of scapula and long bones of unspecified upper limb |
| C40.01 | ICD10CM | Malignant neoplasm of scapula and long bones of right upper limb |
| C40.02 | ICD10CM | Malignant neoplasm of scapula and long bones of left upper limb |
| C40.1 | ICD10CM | Malignant neoplasm of short bones of upper limb |
| C40.10 | ICD10CM | Malignant neoplasm of short bones of unspecified upper limb |
| C40.11 | ICD10CM | Malignant neoplasm of short bones of right upper limb |
| C40.12 | ICD10CM | Malignant neoplasm of short bones of left upper limb |
| C40.2 | ICD10CM | Malignant neoplasm of long bones of lower limb |
| C40.20 | ICD10CM | Malignant neoplasm of long bones of unspecified lower limb |
| C40.21 | ICD10CM | Malignant neoplasm of long bones of right lower limb |
| C40.22 | ICD10CM | Malignant neoplasm of long bones of left lower limb |
| C40.3 | ICD10CM | Malignant neoplasm of short bones of lower limb |
| C40.30 | ICD10CM | Malignant neoplasm of short bones of unspecified lower limb |
| C40.31 | ICD10CM | Malignant neoplasm of short bones of right lower limb |
| C40.32 | ICD10CM | Malignant neoplasm of short bones of left lower limb |
| C40.8 | ICD10CM | Malignant neoplasm of overlapping sites of bone and articular cartilage of limb |
| C40.80 | ICD10CM | Malignant neoplasm of overlapping sites of bone and articular cartilage of unspecified limb |
| C40.81 | ICD10CM | Malignant neoplasm of overlapping sites of bone and articular cartilage of right limb |
| C40.82 | ICD10CM | Malignant neoplasm of overlapping sites of bone and articular cartilage of left limb |
| C40.9 | ICD10CM | Malignant neoplasm of unspecified bones and articular cartilage of limb |
| C40.90 | ICD10CM | Malignant neoplasm of unspecified bones and articular cartilage of unspecified limb |
| C40.91 | ICD10CM | Malignant neoplasm of unspecified bones and articular cartilage of right limb |
| C40.92 | ICD10CM | Malignant neoplasm of unspecified bones and articular cartilage of left limb |
| C41 | ICD10CM | Malignant neoplasm of bone and articular cartilage of other and unspecified sites |
| C41.0 | ICD10CM | Malignant neoplasm of bones of skull and face |
| C41.1 | ICD10CM | Malignant neoplasm of mandible |
| C41.2 | ICD10CM | Malignant neoplasm of vertebral column |
| C41.3 | ICD10CM | Malignant neoplasm of ribs, sternum and clavicle |
| C41.4 | ICD10CM | Malignant neoplasm of pelvic bones, sacrum and coccyx |
| C41.9 | ICD10CM | Malignant neoplasm of bone and articular cartilage, unspecified |
| D48.0 | ICD10CM | Neoplasm of uncertain behavior of bone and articular cartilage |
| Humoral hypercalcemia of malignancy | ||
| E83.52 | ICD10CM | Hypercalcemia |
| Prevention of skeletal related events associated with bone metastases from solid tumor | ||
| C79.51 | ICD10CM | Secondary malignant neoplasm of bone |
| Prevention of skeletal related events in multiple myeloma | ||
| C90.0 | ICD10CM | Multiple myeloma |
| C90.00 | ICD10CM | Multiple myeloma not having achieved remission |
| C90.02 | ICD10CM | Multiple myeloma in relapse |
ICD code information from First Databank (FDB).
Formulary status
Search health-plan coverage for this drug by ZIP code.
Choose the first character of a health plan name.
Last reviewed · Source: First Databank (FDB) drug data
On this page
Actions
Sign in to save favorites
Saving this drug requires a free Physicians Office Resource account.