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Cobimetinib | CAS No: 934660-93-2 | GMP-certified suppliers
A medication that treats unresectable or metastatic melanoma with BRAF mutations and adult histiocytic neoplasms by inhibiting tumor cell proliferation through targeted kinase blockade.
Therapeutic categories
Primary indications
- Cobimetinib is indicated in combination with [vemurafenib] for the treatment of unresectable or metastatic melanoma with a BRAF V600E or V600K mutation
- As a single agent, cobimetinib is also indicated for the treatment of adult patients with histiocytic neoplasms
Product Snapshot
- Cobimetinib is formulated as an oral tablet
- It is primarily used for the treatment of unresectable or metastatic melanoma with specific BRAF mutations and histiocytic neoplasms
- The product is approved for use in the EU, US, and Canada
Clinical Overview
Clinically, cobimetinib is approved in several regions including Switzerland and the United States for use in combination with vemurafenib, a BRAF inhibitor, for the treatment of unresectable or metastatic melanoma harboring BRAF V600 mutations. Additionally, cobimetinib monotherapy has an indication for adult patients with histiocytic neoplasms. The combination therapy addresses the clinical limitation posed by intrinsic and acquired resistance to BRAF inhibition alone; reactivation of the MAPK pathway is a primary resistance mechanism. By concurrently inhibiting both BRAF and MEK kinases, cobimetinib and vemurafenib provide dual pathway blockade, enhancing apoptosis and reducing tumor proliferation.
Pharmacodynamically, cobimetinib binds reversibly to MEK1 and MEK2, suppressing downstream ERK activation and interrupting cell proliferation signals. Preclinical tumor models demonstrate effective growth inhibition of BRAF-mutant cells. Pharmacokinetic data identify cobimetinib as a substrate and inhibitor of multiple cytochrome P450 isoforms, including CYP3A4 and CYP2D6, and as a substrate for transporters such as P-glycoprotein and organic anion-transporting polypeptides (OATP1B1 and OATP1B3). These interactions are relevant to drug-drug interaction potential and patient safety.
Safety considerations include the risk of photosensitivity reactions, consistent with its classification as a photosensitizing agent, and the narrow therapeutic index necessitating careful dose management. Adverse effects and toxicity profiles require vigilant monitoring during treatment.
For API sourcing and quality assurance, manufacturers and procurement specialists should verify compliance with stringent purity and potency standards, given cobimetinib’s complex kinase inhibition profile and narrow therapeutic window. Reliable characterization of the API with respect to residual solvents, stereochemical integrity, and impurity profiles is critical to ensure consistent clinical performance and regulatory compliance.
Identification & chemistry
| Generic name | Cobimetinib |
|---|---|
| Molecule type | Small molecule |
| CAS | 934660-93-2 |
| UNII | ER29L26N1X |
| DrugBank ID | DB05239 |
Pharmacology
| Summary | Cobimetinib is a reversible inhibitor of MEK1 and MEK2, key kinases in the RAS/RAF/MEK/ERK signaling pathway that regulates cellular proliferation. It targets tumors with BRAF V600 mutations by blocking downstream MAPK pathway activation, which is often reactivated in BRAF-inhibitor resistant cancers. Cobimetinib is used in combination with BRAF inhibitors to achieve dual pathway inhibition and enhance antitumor activity. |
|---|---|
| Mechanism of action | Cobimetinib is a reversible inhibitor of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1 (MEK1) and MEK2. MEK proteins are upstream regulators of the extracellular signal-related kinase (ERK) pathway, which promotes cellular proliferation. BRAF V600E and K mutations result in constitutive activation of the BRAF pathway which includes MEK1 and MEK2. In mice implanted with tumor cell lines expressing BRAF V600E, cobimetinib inhibited tumor cell growth. Cobimetinib and vemurafenib target two different kinases in the RAS/RAF/MEK/ERK pathway. Compared to either drug alone, coadministration of cobimetinib and vemurafenib resulted in increased apoptosis in vitro and reduced tumor growth in mouse implantation models of tumor cell lines harboring BRAF V600E mutations. Cobimetinib also prevented vemurafenib-mediated growth enhancement of a wild-type BRAF tumor cell line in an in vivo mouse implantation model. |
| Pharmacodynamics | Cobimetinib is a reversible inhibitor of mitogen-activated protein kinase 1 (MAPK)/extracellular signal-regulated kinase 1 (MEK1) and MEK2. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a BRAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signaling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases. Cobimetinib is used in combination with vemurafenib because the clinical benefit of a BRAF inhibitor is limited by intrinsic and acquired resistance. Reactivation of the MAPK pathway is a major contributor to treatment failure in BRAF-mutant melanomas, approximately ~80% of melanoma tumors become BRAF-inhibitor resistant due to reactivation of MAPK signaling. BRAF-inhibitor-resistant tumor cells are sensitive to MEK inhibition, therefore cobimetinib and vemurafenib will result in dual inhibition of BRAF and its downstream target, MEK. |
Targets
| Target | Organism | Actions |
|---|---|---|
| Dual specificity mitogen-activated protein kinase kinase 1 | Humans | inhibitor |
ADME / PK
| Absorption | Following oral dosing of 60 mg once daily in cancer patients, the median time to achieve peak plasma levels (T<sub>max</sub>) was 2.4 (range:1–24) hours, geometric mean steady-state AUC<sub>0-24h</sub> was 4340 ng∙h/mL (61% CV) and C<sub>max</sub> was 273 ng/mL (60% CV). The absolute bioavailability of COTELLIC was 46% (90% CI: 40%, 53%) in healthy subjects. A high‐fat meal (comprised of approximately 150 calories from protein, 250 calories from carbohydrate, and 500–600 calories from fat) had no effect on cobimetinib AUC and Cmax after a single 20 mg COTELLIC was administered to healthy subjects. |
|---|---|
| Half-life | Following oral administration of COTELLIC 60 mg once daily in cancer patients, the mean elimination half-life (t1/2) was 44 (range: 23–70) hours. |
| Protein binding | Cobimetinib is 95% bound to human plasma proteins in vitro, independent of drug concentration. |
| Metabolism | Cobimetinib is mainly metabolized via CYP3A oxidation and UGT2B7 glucuronidation with no major metabolites formed. |
| Route of elimination | Following oral administration of a single 20 mg radiolabeled cobimetinib dose, 76% of the dose was recovered in the feces (with 6.6% as unchanged drug) and 17.8% of the dose was recovered in the urine (with 1.6% as unchanged drug). |
| Volume of distribution | The estimated apparent volume of distribution was 806 L in cancer patients based on a population PK analysis. |
| Clearance | Following oral administration of COTELLIC 60 mg once daily in cancer patients, the mean apparent clearance (CL/F) was 13.8 L/h (61% CV). |
Formulation & handling
- Cobimetinib is a small molecule drug formulated exclusively for oral administration in tablet form.
- The compound exhibits low water solubility and high lipophilicity (LogP 5.04), requiring careful consideration in formulation to enhance bioavailability.
- Avoid co-administration with grapefruit and St. John's Wort due to CYP3A4-mediated metabolic interactions affecting drug plasma levels.
Regulatory status
| Lifecycle | The active pharmaceutical ingredient is currently protected by multiple patents in the United States, with expiry dates ranging from 2027 to 2036. It is marketed in the EU, US, and Canada, representing a product in a mature but patent-protected phase across these regions. |
|---|
| Markets | EU, US, Canada |
|---|
Supply Chain
| Supply chain summary | Cobimetinib is marketed under a single branded product across the US, EU, and Canadian markets by originator companies holding multiple patents primarily in the United States. Patent protection extends through at least 2027, with some patents lasting until 2036, indicating limited generic competition currently and in the near future. The sustained patent coverage supports ongoing exclusive manufacturing and supply by the original developers. |
|---|
Safety
| Toxicity | The most common adverse effects (>20%) for cobimetinib are diarrhea, photosensitivity reactions, nausea, fever and vomiting. |
|---|
- Handle cobimetinib with appropriate skin and eye protection due to potential photosensitivity reactions
- Use in well-ventilated areas to minimize exposure and potential gastrointestinal irritation
- Avoid inhalation or direct contact to reduce risk of adverse effects such as nausea and fever
Cobimetinib is a type of Protein kinase inhibitors
Protein kinase inhibitors are a vital subcategory of pharmaceutical active pharmaceutical ingredients (APIs) that play a crucial role in targeted cancer therapies. These inhibitors specifically target and block the activity of protein kinases, enzymes that regulate various cellular processes, including cell growth, division, and signal transduction.
Protein kinase inhibitors function by binding to the active site of protein kinases, preventing them from phosphorylating specific proteins and disrupting intracellular signaling pathways. This targeted approach inhibits the uncontrolled growth and proliferation of cancer cells, ultimately leading to their death.
The development of protein kinase inhibitors has revolutionized cancer treatment by providing more effective and less toxic alternatives to traditional chemotherapy. These drugs have demonstrated impressive results in the treatment of various cancers, including lung, breast, and leukemia.
The pharmaceutical industry invests heavily in research and development to discover novel protein kinase inhibitors with improved potency, selectivity, and pharmacokinetic properties. High-throughput screening, computational modeling, and structure-activity relationship studies are employed to identify potential lead compounds.
The success of protein kinase inhibitors in treating cancer has spurred significant interest in this subcategory of APIs. Ongoing research aims to expand their applications to other diseases, such as autoimmune disorders and neurological conditions.
In conclusion, protein kinase inhibitors are a valuable class of pharmaceutical APIs with immense potential for targeted cancer therapies. Continued advancements in this field hold promise for improved treatment outcomes and enhanced patient care.
Cobimetinib (Protein kinase inhibitors), classified under Anticancer drugs
Anticancer drugs belong to the pharmaceutical API (Active Pharmaceutical Ingredient) category designed specifically to combat cancer cells. These powerful medications play a crucial role in cancer treatment and are developed to target and destroy cancerous cells, preventing their growth and spread.
Anticancer drugs are classified based on their mode of action and can include various types such as chemotherapy drugs, targeted therapy drugs, immunotherapy drugs, and hormonal therapy drugs. Chemotherapy drugs work by interfering with the cell division process, thereby inhibiting the growth of cancer cells. Targeted therapy drugs, on the other hand, are designed to attack specific molecules or genes involved in cancer growth, minimizing damage to healthy cells. Immunotherapy drugs stimulate the body's immune system to recognize and destroy cancer cells. Hormonal therapy drugs are used in cancers that are hormone-dependent, such as breast or prostate cancer, to block the hormones that fuel cancer cell growth.
These APIs are typically synthesized through complex chemical processes in state-of-the-art manufacturing facilities. Stringent quality control measures ensure the purity, potency, and safety of these drugs. Anticancer APIs undergo rigorous testing and adhere to stringent regulatory guidelines before being approved for clinical use.
Due to their critical role in cancer treatment, anticancer drugs are in high demand worldwide. Researchers and pharmaceutical companies continually strive to develop new and more effective APIs in this category to enhance treatment outcomes and minimize side effects. The ongoing advancements in the field of anticancer drug development offer hope for improved cancer therapies and better patient outcomes.
Cobimetinib API manufacturers & distributors
Compare qualified Cobimetinib API suppliers worldwide. We currently have 1 companies offering Cobimetinib API, with manufacturing taking place in 1 different countries. Use the table below to review supplier type, countries of origin, certifications, product portfolio and GMP audit availability.
| Supplier | Type | Country | Product origin | Certifications | Portfolio |
|---|---|---|---|---|---|
| Senova Technology Co., Lt... | Producer | China | China | CoA, GMP, ISO9001, USDMF | 157 products |
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