Perhaps something to track over time:
ROCK inhibitors have potential therapeutic applicability in a wide variety of pathological conditions including asthma, cancer, erectile dysfunction, glaucoma, insulin resistance, kidney failure, neuronal degeneration, and osteoporosis.
I’ve been interested in this topic for a while. Statins are Rho-kinase inhibitors (one type more than the other, as research points out). It has been suggested in quite some studies that these suppressive effects on Rho kinase signalling of statins, may be underlying many of their pleiotropic effects.
ROCK inhibition may explain the benefits of Reishi mushrooms.
With regard to “clinical applications for anti-erectile dysfunction”, ROCK inhibition seems to be the mechanism of action of Tongkat Ali, the Malaysian natural Viagra.
How do ROCK inhibitors affect lifespan?
ROCK (Rho-associated protein kinase) inhibitors may affect lifespan in the following ways:
• Reduced cell senescence: ROCK inhibitors suppress the activity of Rho GTPases, which are involved in regulating cell senescence. By reducing Rho GTPase activity, ROCK inhibitors could decrease senescent cellular changes that occur with aging and shorten lifespan. This may help slow the aging process and increase lifespan.
• Stabilized cytoskeleton: ROCK inhibitors also stabilize the cytoskeleton, which can become unstable with aging. By preserving cytoskeletal stability, ROCK inhibitors may reduce cytoskeletal aging and dysfunction that contribute to cellular decline with aging. This could have lifespan-extending effects.
• Decreased inflammation: In addition, ROCK inhibitors dampen inflammation by blocking the effects of Rho GTPases, which regulate inflammatory processes. Lowering inflammation may slow age-related degeneration and increase longevity.However, more research is needed to directly determine how ROCK inhibitors influence aging and lifespan. These inhibitors target specific aspects of Rho GTPase signaling, but may have other effects that could either increase or decrease lifespan. Further study is required to fully understand the impacts of ROCK inhibitors on aging and lifespan, and how they can be safely used to promote longevity. Overall, ROCK inhibitors hold promise for slowing aging, but their effects on lifespan would depend on their particular biological activities and consequences.
https://pubs.acs.org/doi/full/10.1021/acsnano.5c11482#
Short version: CEPT keeps fragile, lonely neurons alive by shutting down multiple early-death programs at once, while a plain ROCK inhibitor just stops them from ripping themselves apart the first couple days. After that, cells need more than “less blebbing.” They need translation, anti-apoptosis, and general stress control. CEPT covers all of it; ROCKi doesn’t.
What each part is doing (stacked effects):
• Chroman-1 (the “C”): a more potent ROCK1/2 inhibitor than the usual Y-27632. It reduces actomyosin tension and membrane blebbing, so cells attach and don’t die of dissociation-induced anoikis. Helpful in days 0–2, but not a full survival plan. 
• Emricasan (the “E”): pan-caspase blocker that directly suppresses the executioner phase of apoptosis while the cells are still stressed and isolated. Think “you can’t press the self-destruct button if I removed the button.” 
• Polyamines (the “P”): stabilize RNA and membranes, tune translation and autophagy, and generally buffer stress. They make the cellular housekeeping less chaotic while synapses and adhesions mature. 
• trans-ISRIB (the “T”): disables the integrated stress response by re-activating eIF2B, so protein synthesis keeps running instead of shutting down into stress-granule sulking. That’s crucial after day 2–3 when neurons must synthesize a lot of proteins to grow neurites and form circuits. 
Why CEPT outlasts ROCKi:
• Early on, survival is limited by mechanical/cytoskeletal shock from dissociation. ROCK inhibition fixes that, which is why you see a benefit through about day 5. After that, limiting factors shift to translation capacity, mitochondrial and ER stress, and caspase-mediated pruning. CEPT hits all those layers, so the benefit persists as cells transition from “don’t die” to “build networks.” 
Empirical backdrop:
• The original CEPT work showed markedly higher survival and cloning efficiency for single cells by combining ROCKi with caspase inhibition, polyamines, and ISR blockade. It was discovered via high-throughput screening, then validated across passaging, cloning, gene editing, and organoid contexts. In multiple follow-ups, CEPT improves aggregation quality and long-term tissue fitness, not just day-1 stickiness. 
So yes: ROCKi calms the immediate drama; CEPT keeps the lights on, the kitchen stocked, and the construction crew paid until the “circuit” is actually built. Biology is needy like that.