Congenital cases may have developmental abnormality due to abnormal muscle structure, usually muscle atrophy / hypertrophy or rarely, absence of the muscle and incorrect placement. Specific & common causes include:

Superior oblique Palsy / Congenital fourth nerve palsy
Inferior oblique overaction
Browns syndrome
Duanes retraction syndrome
Double elevator palsy
Fibrosis of rectus muscle in Graves Disease (most commonly inferior rectus is involved)
Surgical trauma to the vertical muscles (e.g. during scleral buckling surgery or cataract surgery causing iatrogenic trauma to the vertical muscles).Sudden onset hypertropia in a middle aged or elderly adult may be due to compression of the trochlear nerve and mass effect from a tumor, requiring urgent brain imaging using MRI to localise any space occupying lesion. It could also be due to infarction of blood vessels supplying the nerve, due to diabetes and atherosclerosis. In other instances it may be due to an abnormality of neuromuscular transmission, i.e., Myasthenia Gravis. Treatment
In general, strabismus can be approached and treated with a variety of procedures. Depending on the individual case, treatment options include:

Correction of refractive errors by glasses
Prism therapy (if tolerated, to manage diplopia)
Vision Therapy
Patching (mainly to manage amblyopia in children and diplopia in adults)
Botulinum toxin injection
Surgical correctionSurgical correction of the hypertropia is desired to achieve binocularity, manage diplopia and/or correct the cosmetic defect. Steps to achieve the same depend on mechanism of the hypertropia and identification of the offending muscles causing the misalignment.
Cobicistat is a potent inhibitor of cytochrome P450 3A enzymes, including the important CYP3A4 subtype. It also inhibits intestinal transport proteins, increasing the overall absorption of several HIV medications, including atazanavir, darunavir, and tenofovir alafenamide. Chemistry
Cobicistat is a drug analogue of ritonavir, in which the valine moiety is exchanged for a 2-morpholinoethyl group, and the backbone hydroxyl group is removed. These changes effectively eliminate the anti-HIV activity of ritonavir while preserving its inhibitory effects on the CYP3A isozyme family of proteins. Cobicistat is therefore able to increase plasma concentration of other coadministered anti-HIV drugs without the risk of causing cobicistat-resistant mutations in the HIV virus. Synthesis
Cobicistat may be synthesized from any number of commercially available starting materials. The synthesis shown below utilizes L-methionine and bromoacetic acid as starting materials. Discovery and development
Cobicistat was developed through structure-activity relationship studies using ritonavir and desoxyritonavir as lead compounds. These studies were conducted by scientists at Gilead Sciences, and successfully optimized ritonavir into a potent CYP3A inhibitor lacking anti-HIV activity. Cobicistat shows potent, selective inhibition of the CYP3A isozyme family (IC50 0.15 μM) compared to some CYP1A and CYP2C isozymes. As cobicistat was discovered using structure-activity relationship studies, its CYP3A binding is still poorly understood; however, research on the protein-ligand interactions between CYP3A4 and ritonavir analogues demonstrates that CYP 3A4 residues Ile369, Ala370, Met371, as well as Arg105 and Ser119, play an important role in ritonavir analogue inhibition of CYP3A4. References
External links
"Cobicistat". Drug Information Portal. U.S. National Library of Medicine.